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max slope
kidney
max D1=T1
aorta
8
This formula states that RBF per unit volume can
be calculated using the maximum rate of contrast
uptake by the kidney and the maximum contrast-
induced change in relaxivity in the aorta. The authors
converted signal intensity to T1 using an in vitro
phantom-derived relationship between signal inten-
sity and T1.
Vallee et al [17] used this method to measure
cortical and medullary blood flow in 27 patients in
three patient groups: (1) normal renal function as
determined by serum creatinine level, (2) RAS, and
(3) renal failure. They found low cortical blood flow
in those patients with RAS compared with those with
normal renal function and low cortical and medullary
A.J. Huang, V.S. Lee / Radiol Clin N Am 41 (2003) 10011017 1004
blood flows in those patients with renal failure
compared with those with normal renal function.
Values calculated were comparable with published
RBF measurements obtained using other modalities,
including dynamic CT,
133
Xe washout, and positron
emission tomography.
Renal perfusion imaging using intravascular contrast
agents
Although assumptions about the limited extent
of extravascular leakage of contrast during initial
enhancement may be valid, intravascular agents are
preferable for the measurement of renal perfusion.
Prasad et al [21] investigated renal cortical perfu-
sion imaging using an exogenous intravascular
contrast agent, MS-325, which binds to albumin
after injection. The group acquired MS-325
enhanced perfusion images with a turbo FLASH
sequence in seven pigs that underwent surgically
induced RAS, and they expressed regional blood
flow as the ratio of regional blood volume to indi-
cator mean transit time. MR imaging measurements
of renal perfusion were consistent with microsphere
measurements, but a slight elevation of the former
may represent a limitation of this technique. Inter-
estingly, there was minimal decrease in renal per-
fusion even in the face of severe RAS, possibly
related to the kidneys innate capacity to regulate
blood flow. Although these results are encouraging,
intravascular contrast agents have yet to be ap-
proved for RBF measurement.
Renal perfusion imaging using arterial spin labeling
techniques
An alternative approach to measuring renal perfu-
sion with exogenous contrast agents uses arterial spin
labeling techniques, and early results have been prom-
ising. Prassad et al [22] studied the efficacy of using
both signal targeting with alternating radiofrequency
(STAR) angiography and STAR with echo-planar
imaging for readout (EPISTAR) perfusion imaging
to characterize surgically created RAS in pigs.
EPISTAR imaging revealed decreased signal intensi-
ties in kidneys supplied by stenotic renal arteries.
Moreover, correlating the perfusion images with con-
ventional selective angiograms showed that segmental
regions demonstrating reduced signal intensity were
supplied by occluded branch vessels. When the
authors used the typical criterion of 70% stenosis by
conventional angiography to indicate a positive study,
the differences in signal intensity curves were 100%
sensitive and 100% specific for the detection of renal
perfusion abnormalities. Furthermore, differences in
these curves were more pronounced in the presence of
a vasodilator such as acetylcholine, which is consistent
with the results of other investigators [23,24].
Other groups have reported similarly promising
results using different methods [25,26]. Although
these studies show that using MR imaging to quantify
renal perfusion is feasible, no group has validated
these methods against an accepted standard, and these
methods have not been commercially implemented for
widespread use. Further investigation is warranted.
Renal perfusion imaging using blood oxygenation
level dependent imaging
Blood oxygenation level dependent (BOLD) im-
aging relies on the different magnetic properties of
oxyhemoglobin and deoxyhemoglobin to achieve tis-
sue contrast on T2*-weighted images [27]. Although
BOLDimaging has been used to measure perfusion, its
value in renal applications may reside in its capacity to
quantify oxygen use noninvasively. BOLD imaging is
particularly suited for assessing oxygenation of the
renal medulla, which normally functions at hypoxic
levels [28]. Prasad et al [27,29] used BOLDimaging to
study the effects of furosemide, acetazolamide, and
water diuresis on renal oxygenation in 12 healthy
volunteers. They found that furosemide decreased
medullary R2* (1/T2*) in all patients, indicating an
increase in medullary oxygenation, but it did not
significantly affect cortical R2*. The furosemide-in-
duced decrease in activity, and hence oxygen use, of
proximal tubular transporters explains these findings
[27]. Acetazolamide did not significantly affect corti-
cal or medullary R2*. Water diuresis had similar
effects on the cortex and medulla as furosemide,
although the authors hypothesized in this case that
the findings were caused by changes in regional blood
flow [27].
These preliminary studies illustrate the potential
for BOLD imaging to assess renal medullary oxy-
genation noninvasively; however, this technique has
a limited capacity for determining whether changes in
oxygenation are caused by differences in blood flow
or differences in oxygen use [30].
Glomerular filtration rate
Monitoring renal function is essential in many
causes of acute and chronic renal insufficiency to
assess prognosis, response to treatment, progression
of disease, and nephrotoxicity associated with thera-
peutic agents. Clinicians often use serum creatinine
A.J. Huang, V.S. Lee / Radiol Clin N Am 41 (2003) 10011017 1005
levels or creatinine clearance for this purpose, because
measuring them is relatively easy and safe. Serum
creatinine, however, is an insensitive indicator of renal
dysfunction; its production varies across individuals,
and diet and medications can affect its kinetics [31].
Clearances of inulin and DTPA are indicators of GFR
and are better markers of renal function, but these
measurements require multiple blood and urine col-
lections, and they do not provide unilateral renal
functional information.
For less invasive measurements of renal function
using MR imaging, early work showed that even
without contrast administration, the loss of cortico-
medullary differentiation on T1-weighted MR imag-
ing indicated a serum creatinine level greater than
3 mg/dL [32]. Recently, several MR imaging tech-
niques for the noninvasive measurement of single
kidney GFR have been developed based on the
imaging of the renal uptake of gadolinium chelates.
Three categories of GFR measurements using MR
imaging are reviewed: (1) global GFR determination
using blood clearance of gadolinium-based contrast
agents, (2) single kidney GFR determination using
MR relaxometry, and (3) single kidney GFR deter-
mination using intrarenal kinetics.
Global GFR using blood clearance of
gadolinium-based contrast agents
In their 1992 paper, Choyke et al [33] compared
global GFR determined by clearance of
99m
TcDTPA
(GFR
Tc
) with that determined by clearance of
Gd-DTPA (GFR
Gd
) in 90 patients based on three
separate urine and blood samples using the stan-
dard equation
GFR
tracer
tracer
urine
V
tracer
plasma
; 9
where V is the urine flow rate, and [tracer]
x
is the
concentration of tracer in x.
The authors calculated Gd-DTPAconcentrations in
urine and plasma by first determining the T1 of each
fluid using an nuclear magnetic resonance (NMR)
spectrometer and then using an experimentally derived
relationship to convert T1 into Gd-DTPA concentra-
tion. GFR
Gd
correlated well with GFR
Tc
(correlation
coefficient = 0.94), and the coefficient of variation of
their differences was 3.6%. Ros et al [1] performed a
similar study that combined plasma Gd-DTPA clear-
ance estimates of GFR with MR angiography and MR
renography. Across six patients, GFR
Gd
and GFR
Tc
correlated well (correlation coefficient = 0.98), and the
standard error was 3.85 mL/minute. Although clear-
ance of Gd-DTPAcan be used to measure global GFR,
the use of NMR spectrometers and the repeated
sampling of blood and urine required preclude wide-
spread clinical use.
Single kidney GFR using MR relaxometry
Although Gd-DTPA clearance was the basis of the
global GFR studies previously mentioned, an alter-
native approach enables the measurement of single
kidney GFR based on calculations of the single
kidney extraction fraction (EF) of a tracer like inulin
or Gd-DTPA. The method is based on imaging and
does not require blood or urine collection. EF is
defined as
EF
tracer
tracer
artery
tracer
vein
tracer
artery
10
Equation 1 relates observed T1 in a tissue to
gadolinium concentration. Rearranging and substitut-
ing equation 1 into equation 10, we get
EF
Gd
T1
precontrast
T1
vein
T1
vein
T1
artery
T1
precontrast
T1
artery
11
Once EF is determined, GFR can be calculated
according to the following.
GRF EF RBF 1Hct; 12
where RBF is renal blood flow and Hct is hematocrit.
Three groups have published results using this
approach to measure single kidney GFR [3436].
Dumoulin et al [34] tested this approach on human
volunteers and calculated EF using an inversion
recovery sequence to determine the T1 values of
moving blood in the renal artery and renal vein.
The EFs obtained in the study spanned a wide range
and were inconsistent with data published in previous
clearance studies, but it was believed that clearance
studies were unsuitable for judging the EFs and GFRs
calculated with this method.
Niendorf et al [35] performed a study to validate
this technique against single kidney inulin clearance
measurements in six pigs. The inversion recovery
sequence they used to obtain T1 measurements, based
on a Look-Locker method [11], was modified to use
GRE or EPI readout pulses for measuring relaxation
recovery. Several advantages resulted from this ap-
proach, including decreased sensitivity to off-reso-
nance effects, the use of large readout pulses, and
increased vessel contrast [35]. The group used the
A.J. Huang, V.S. Lee / Radiol Clin N Am 41 (2003) 10011017 1006
renal vein to derive renal venous T1 and the inferior
vena cava to approximate renal arterial T1, and they
measured RBF using phase-contrast flow quantifica-
tion MR imaging in the renal artery or renal vein.
Although GRE imaging provided better spatial reso-
lution, EPI was faster and facilitated breathhold
acquisitions. EF
Gd
and GFR
Gd
correlated well with
EF
inulin
and GFR
inulin
(linear regression slopes for
measuring GFR were 0.81 and 0.85 for GRE and EPI
techniques, respectively), and their respective differ-
ences were statistically insignificant.
Coulam et al [36] used a similar technique to
examine the effects of RAS on EF and GFR in a pig
model. MR imaging sequence modifications included
cardiac gating, adiabatic inversion, interleaved spiral
readouts, and spectral-spatial excitation pulses. The
authors measured T1 relaxation using cardiac-gating
during suspended respiration and approximated arte-
rial input T1 using either the inferior vena cava or the
aorta, and they obtained RBF with phase-contrast
imaging of the renal arteries. EF
Gd
and EF
inulin
corre-
lated well (correlation coefficient = 0.77, P< 0.01),
although EF
Gd
values were 22% less than EF
inulin
( P = 0.01). In this study, the authors completed all
calculations of EF
inulin
before computing EF
Gd
, and
they hypothesized that the additional anesthesia time
coupled with declining renal function adversely af-
fected EF
Gd
. In the kidneys with RAS, EF
Gd
, EF
inulin
,
RBF, and GFR were all significantly reduced.
This approach to measuring single kidney GFR is
innovative, but it faces several technical challenges,
including difficulties estimating gadolinium concen-
tration and determining RBF using phase-contrast
flow measurements in small vessels.
Single kidney GFR based on intrarenal kinetics
Gadolinium chelates traverse the kidney in a pre-
dictable fashion, progressing from the arterial blood to
the cortex, medulla, and collecting system. This re-
flects the normal passage of these substances through
the nephron from the glomerular capillary through
Bowmans capsule into the proximal convoluted tu-
bule (cortex), through the loop of Henle (medulla), the
distal convoluted tubule, the collecting duct (cortex
and medulla), and finally through the renal calyx. If
one considers gadolinium chelates to be tracers whose
passage through the kidney reflects the behavior of
other glomerular agents, then one can apply tracer
kinetic models to interpret patterns of intrarenal
enhancement in terms of parameters, such as GFR.
Baumann and Rudin [6] proposed a first-order
kinetic model of the kidney that consists of two
compartments, the cortex and medulla, and a rate
constant between the two representing the rate of
clearance of tracer from the cortex.
dGd
m
dt
k Gd
c
; 13
where [Gd]
m,c
are the time-varying concentrations of
gadolinium in the medulla and cortex, respectively,
and k is the flow rate between compartments.
In normal rats, the authors compared MR renogra-
phy images acquired with a rapid acquisition with
relaxation enhancement sequence with those acquired
with a snapshot sequence, using gadolinium tetraazo-
cyclododecane-tetraacetate (Gd-DOTA), a glomerular
contrast agent. The group converted signal intensities
to T1 values using available formulas relating signal
intensity to T1 for the rapid acquisition with relaxation
enhancement and snapshot sequences, computed
Gd-DOTA concentration from T1 values using equa-
tion 1, and determined k by fitting the resulting corti-
cal and medullary Gd-DOTA concentration curves to
equation 13. The snapshot sequence produced superior
images compared with the rapid acquisition with relax-
ation enhancement sequence and was less affected by
susceptibility effects at high Gd-DOTA concentra-
tions. Using the snapshot sequence, the derived k
was 3.4 F 0.5 minutes
1
. Although plotting the initial
rate of increase of Gd-DOTA concentration in the
medulla against the administered dose of Gd-DOTA
did indeed reveal a linear dependence, lending support
to the proposed first-order kinetic model of glomerular
filtration, establishing the accuracy of this technique
requires comparison to a reference standard.
Laurent et al [37] used Baumann and Rudins [6]
first-order kinetic model and a snapshot sequence to
calculate GFR
Gd
in their study of the effects of
hypertension on renal function in rats. A few days
after the MR imaging experiment, they compared
GFR
inulin
, calculated from the clearance of [
3
H]inulin
using equation 9, with GFR
Gd
. GFR
Gd
and GFR
inulin
correlated well in the 17 rats studied (correlation
coefficient = 0.75).
Smith et al [38] estimated GFR using a different
two-compartment model, which was confined to the
cortex. In their model, the arteries and capillaries form
the first compartment, and the proximal convoluted
tubules form the second. Two rate constants, k
in
and
k
out
, describe the flow into and out of the proximal
tubules; k
in
represents GFR. The authors generated a
renal cortical Gd-DOTA concentration curve using a
two-dimensional cardiac-gated fast T1-weighted
spoiled GRE sequence following a 0.05 mmol/kg
injection of Gd-DOTA and fitted it to this model to
estimate GFR. For the four patients studied with this
A.J. Huang, V.S. Lee / Radiol Clin N Am 41 (2003) 10011017 1007
approach, GFR ranged from 16 to 71 mL/min/100 g of
kidney cortex. Although these values are similar to
values reported in the literature, validating this method
against established standards remains to be done.
The authors group has described initial results
with a more expansive multicompartmental model of
the entire vascular-nephron system [39]. The model
considers the distinct cortical and medullary functional
nephron units (artery-capillary, proximal convoluted
tubule, loop of Henle, distal convoluted tubule, col-
lecting duct, and calyces-ureter) as separate compart-
ments (Fig. 2). The cortex, medulla, and collecting
system are then expressed as a linear combination of
these compartments. A series of first-order differential
equations models the course of Gd-DTPA through
pairs of compartments over time. Like Smith et als
k
in
[38], the rate constant describing the passage of
Gd-DTPA from the arteries and capillaries to the
proximal tubules represents GFR. Using a fast three-
dimensional MR renography technique, the authors
implemented this model and computed GFRin a series
of nine subjects (18 kidneys) and found good correla-
tion (correlation coefficient = 0.76) with same-day
gamma camera and blood clearancederived mea-
sures of single kidney GFR using
99m
TcDTPA [40].
One advantage of this model over previous ones is its
inclusion of renal structures distal to the proximal
tubules. In principle, this model can assess tubular
physiology and pathology based on MR renogra-
phy, both of which have been almost impossible to
evaluate noninvasively.
Angiotensin converting enzyme inhibitor MR
renography for RVD
Of the 60 million people with hypertension, an
estimated 1% to 5% have RVD as the underlying
cause [41]. As one of the few potentially curable
causes of hypertension, RVD remains an important
yet challenging diagnosis. Not all patients with RAS
have RVD; in fact, those with essential hypertension
tend to develop accelerated atherosclerosis, which
can lead to RAS. These diagnostic limitations have
generated controversies surrounding treatment. Van
Jaarsveld et al [42] concluded from their multicenter
trial that treating hypertension secondary to RVD
with balloon angioplasty was not much better than
treating it with medicine alone, although the criterion
they used for RVD (RAS causing only greater than
50% narrowing) may undermine their conclusions.
Most anatomic tests, such as conventional angi-
ography, MR angiography, and CT angiography, are
limited in their ability to diagnose RVD because they
rely on RAS as the sole criterion. Angiotensin con-
verting enzymeinhibitor (ACE-I) renal scintigraphy
is the best predictor of response to therapy because it
is a functional test of renal ischemia. It does not,
however, supply anatomic information needed for
therapeutic planning.
When performed with MR angiography, MR
renography has the potential to provide an anatomic
and functional evaluation of RVD. Preliminary data
are encouraging, although small sample sizes and
susceptibility effects from concentrated contrast in
the medulla and collecting system as a result of
standard doses of gadolinium have limited early
studies [1,43,44]. In a study of 10 patients, Ros et al
[1] used a turbo FLASH sequence with 0.05 mmol/kg
of Gd-DTPA and time-of-flight MR angiography to
diagnose RAS. They described one patient in whom
severe left RAS shown by conventional angiography
corresponded to decreased left medullary enhance-
ment depicted on MR renography. Using 0.1 mmol/kg
or more of gadolinium, Grenier et al [43] observed a
band of low signal intensity on T1-weighted images
Fig. 2. Multicompartmental model of the vascular-nephron system for analysis of MR renography data in terms of physiologic
parameters. Compartments of the model are intended to reflect closely the anatomy and function of the nephron. Solid arrows
indicate the passage of plasma or tracer-containing tubular fluid between compartments at flow rates Q
ij
, whereas dotted arrows
indicate tracer-free fluid resorption, F
i
, fromthe tubular compartments into the vasa recta. Q
PA
= GFR. (FromLee VS, et al. Analysis
of dynamic three-dimensional (3D) MRrenography: regional characterization by multicompartmental modeling. In: Proceedings of
the International Society for Magnetic Resonance in Medicine. Glasgow, Scotland, UK: 2001. p. 2059; with permission.)
A.J. Huang, V.S. Lee / Radiol Clin N Am 41 (2003) 10011017 1008
that progressed centripetally over the course of more
than 4 minutes. The susceptibility effects of con-
centrated gadolinium in the medulla and collecting
system caused this signal loss and precluded con-
trast quantification.
The successful use of an ACE-I (such as capto-
pril) in renal scintigraphy is the basis for its in-
corporation into MR renography protocols [3].
Decreased renal perfusion pressure in patients with
RAS activates the renin-angiotensin system and
increases production of angiotensin II. Angiotensin
II causes vasoconstriction of the efferent glomerular
arteriole and restores renal perfusion pressure and
glomerular filtration to normal or near-normal levels.
This compensated RAS may not manifest any per-
fusion or filtration abnormalities on renal scintigra-
phy or MR renography. Administering an ACE-I
lowers GFR in the setting of RVD because it blocks
the production of angiotensin II, which decreases
efferent glomerular arteriolar vasoconstriction and
reduces perfusion pressure.
Prasad et al [45] used captopril MR renography
to evaluate the hemodynamic significance of uni-
lateral RAS in their porcine model. They performed
T1-weighted MR renography using a three-dimen-
sional fast imaging with steady state precession
sequence and a 0.1 mmol/kg bolus of Gd-DTPA.
The authors showed that the signal intensity curves
of the right versus left kidneys differed little in the
absence of captopril. Following captopril administra-
tion, however, the kidney supplied by the stenotic
renal artery demonstrated little washout of Gd-DTPA
during the imaging period. These results are consis-
tent with those of ACE-I renal scintigraphy.
The authors group implemented an ACE-I MR
renography protocol combined with MR angiography
in 32 patients with suspected RVD [3]. Imaging
consisted of a two-dimensional turbo FLASH se-
quence using a 2-mL (0.013 mmol/kg) dose of
Gd-DTPA for MR renography followed by con-
trast-enhanced MR angiography using a standard
(0.14 mmol/kg) dose of Gd-DTPA. It was found
that patients with elevated serum creatinine levels
( 2 mg/dL) had depressed cortical and medullary
signal intensities at 1 to 4 minutes following Gd-DTPA
injection when compared with patients with normal
serum creatinine levels ( < 2 mg/dL) (Fig. 3). Effects
of the ACE-I on cortical and medullary enhancement
depended on the presence of RAS and the serum
creatinine level. In patients with RAS, medullary
enhancement following ACE-I administration was
slightly less than in those patients without RAS
( P values ranged from 0.1 to 0.2), whereas there was
no such difference without ACE-I administration.
Patients with elevated serum creatinine levels had
depressed enhancement regardless of the presence or
absence of RAS and regardless of ACE-I administra-
tion. This inability to further characterize RVD in
Fig. 3. Renal cortical (A) and medullary (B) relative signal intensity curves with standard error bars. Patients with serum
creatinine less than 2 mg/dL (solid line) are compared with those with elevated serum creatinine (dotted line). Decreased
medullary enhancement over 1 to 3 minutes in patients with renal insufficiency (dotted line, B) reflects less Gd-DTPA filtered at
the glomerulus and less passing into the loop of Henle (medulla). (From Lee VS, et al. MR renography with low-dose
gadopentetate dimeglumine: feasibility. Radiology 2001;221:3719; with permission.)
A.J. Huang, V.S. Lee / Radiol Clin N Am 41 (2003) 10011017 1009
patients with renal insufficiency represents a limita-
tion of this approach. Among patients with normal
serum creatinine levels, however, ACE-I administra-
tion did unmask decreased GFR by depressing med-
ullary enhancement in patients with RAS (Fig. 4).
ACE-I MR renography may even be useful in
transplant RAS. Sharma et al [46] studied the role of
ACE-I MR renography in 11 post renal transplant
patients with hypertension. They performed ACE-I
MR renography using a turbo FLASH sequence and a
2-mL dose of Gd-DTPA in conjunction with three-
dimensional phase-contrast MR angiography of the
transplant renal arteries. In patients with less than
40% RAS, cortical signal intensity curves before and
after injection of 50 mg of captopril did not differ
significantly. The cortical signal intensity curves of
patients with at least 40% RAS had a lower peak than
those of patients with less than 40% RAS; captopril
exaggerated these differences.
These results illustrate the promise of ACE-I MR
renography for evaluating hemodynamically signifi-
cant RAS, although whether or not this technique is
superior to conventional anatomic studies in its
ability to predict a response to revascularization
remains debatable.
MR urography for hydronephrosis
Hydronephrosis is dilatation of the renal collect-
ing system. It may be congenital or acquired, ob-
structive or nonobstructive, and clinically significant
or insignificant. The goals of the imaging evaluation
of hydronephrosis are threefold: (1) delineation
of the extent of dilatation of the collecting system;
(2) diagnosis of an obstructing cause, if any; and
(3) evaluation of its effects on renal function. Many
imaging modalities have been applied to this prob-
lem. Both ultrasound and IVU primarily evaluate the
morphology of the urinary tract and have difficulty
distinguishing dilated and obstructed urinary tracts
from those that are merely dilated. Diuretic renal
scintigraphy, despite its poor spatial resolution, can
contribute functional information to the assessment,
but the test suffers an unacceptably high false-posi-
tive rate [47]. Contrast-enhanced CT can provide
functional information and excellent anatomic infor-
mation, but the cost of the necessarily high radiation
doses is problematic, particularly in the pediatric
population, and the risk of nephrotoxicity associated
with iodinated contrast agents is unsuitable for those
with renal insufficiency. Faster imaging and non-
nephrotoxic contrast agents have rendered MR imag-
ing increasingly applicable for the evaluation of
genitourinary diseases in general and hydronephrosis
in particular [8,4850]. In addition, MR imaging
eliminates the exposure to ionizing radiation and
nephrotoxic agents inherent in the other modalities.
These imaging strategies are collectively termed
MR urography. Not surprisingly, lessons learned
from interpreting IVU or CT studies readily apply to
the interpretation of MR imaging studies (Fig. 5).
Wen et al [7] studied the effectiveness of Gd-
DTPAenhanced MR imaging in assessing the func-
tion of three classes of rat kidneys: (1) nonobstructed
control, (2) partially obstructed, and (3) completely
obstructed. They acquired GRE images following the
injection of 1 mL/kg of Gd-DTPA. The partially
obstructed kidneys demonstrated delayed contrast
enhancement and washout when compared with the
normal controls. These changes were more pro-
nounced in the completely obstructed kidneys, where
there was continued accumulation of contrast in the
cortex and medulla and delayed appearance of con-
trast in the collecting system. These findings are
analogous to the classic delayed nephrogram and
Fig. 4. Middle-aged hypertensive woman with mild left RAS by MR angiography (arrowhead). MR renography shows normal
medullary enhancement at baseline and decreased medullary enhancement following angiotensin converting enzyme inhibitor
injection, implying significant stenosis. (Modified from Lee VS, et al. MR renography with low-dose gadopentetate dime-
glumine: feasibility. Radiology 2001;221:3719; with permission.)
A.J. Huang, V.S. Lee / Radiol Clin N Am 41 (2003) 10011017 1010
delayed pyelogram observed during the IVU and CT
evaluations of obstructive hydronephrosis.
MR urography is superior to other modalities
because it provides better anatomic and functional
imaging in a single setting. Rohrschneider et al [48]
compared MR urography with a combination of
ultrasound, diuretic renal scintigraphy, and IVU for
the evaluation of 20 piglets that underwent surgically
induced urinary tract obstruction. They performed
static MR imaging using a T2-weighted three-dimen-
sional inversion recovery turbo spin echo sequence,
dynamic MR imaging using a two-dimensional
T1-weighted GRE sequence using 0.1 mmol/kg of
Gd-DTPA and 0.3 mg/kg of furosemide for distention
of the urinary tract, and diuretic renal scintigraphy
using
99m
Tc mercaptoacetyltriglycine and 0.5 mg/kg
of furosemide. MR urography showed the level of
stenosis and the more proximal urinary tract in all
of the cases, whereas IVU showed the same in only
half of the cases. Ultrasound almost never showed
Fig. 5. MR images of a 64-year-old man with a history of bladder cancer cystectomy and neobladder construction. (A) A
coronal single-shot T2-weighted image shows left-sided hydronephrosis and is suspicious for obstruction. (B) A slightly more
anterior image from the same coronal T2-weighted acquisition again shows dilatation of the renal calyces and ureterectasis.
(C) A coronal maximum intensity projection of a Gd-DTPAenhanced three-dimensional spoiled GRE acquisition obtained
5 minutes after intravenous injection of gadolinium shows prompt excretion into the dilated collecting system, indicating
absence of functional obstruction.
A.J. Huang, V.S. Lee / Radiol Clin N Am 41 (2003) 10011017 1011
the level of stenosis. MR urography was also supe-
rior to IVU and ultrasound in demonstrating the
urinary tract distal to the stenosis. A distinct advan-
tage of MR urography was its ability to detect other
findings, such as various fluid collections (using the
static sequence) and their causes (using the dynamic
sequence to depict contrast extravasation). The
authors used signal intensity curves to characterize
relative renal function and urinary excretion, the
results of which agreed well with results obtained
using diuretic renal scintigraphy.
Katzberg et al [8] also investigated the quantita-
tive analysis of MR renography data in their ana-
tomic and functional evaluation of the kidneys of
11 patients with suspected unilateral hydronephrosis.
MR renography images consisted of three 8-mm thick
coronal sections acquired with a fast spoiled GRE
sequence following injection of 0.05 to 0.5 mmol/kg
of gadolinium-based contrast. Although the small
size and modest number of cases of obstructive
hydronephrosis limited this study, the medullary
enhancement pattern was delayed in hydronephrotic
compared with normal kidneys. Whether a qualitative
interpretation of MR renography requires supplemen-
tation with quantitative analysis to diagnose func-
tional obstruction, however, remains to be established.
A related application is the differentiation of
hydronephrosis from pyonephrosis, which is not
always straightforward. The typical diagnostic criteria
used are sonographic (an anechoic calyceal system in
the former and a heterogeneously echoic calyceal
system in the latter), but these are not reliable [51].
Conventional MR imaging also has difficulty sepa-
rating the two conditions, because both often appear
hypointense on T1-weighted images and hyperintense
on T2-weighted images. Chan et al [51], using
diffusion-weighted imaging to study 12 consecutive
patients with pelvicaliectasis detected by ultrasound,
found that hydronephrotic collecting systems had
significantly higher apparent diffusion coefficients
than pyonephrotic collecting systems at a b-factor
of 1000 s/mm
2
(mean apparent diffusion coefficients
= 2.98 F0.65 10
3
mm
2
/s versus 0.64 F0.35
10
3
mm
2
/second, P< 0.001).
MR imaging for renal transplant evaluation
Complications following renal transplantation are
generally categorized as surgical or medical. Surgical
complications usually manifest themselves in the
immediate or early postoperative period and include
RAS and subsequent infarction, renal vein thrombo-
sis, urinary leak, and lymphocele. Typical findings
for these entities on conventional MR imaging have
been described [5255]. Medical complications are
diagnostically more problematic. They include acute
allograft rejection; chronic allograft rejection; acute
tubular necrosis; cyclosporine A toxicity; infection;
and transplant-associated malignancies (lymphoma
and posttransplant lymphoproliferative disorder)
[52]. In the early posttransplant period, acute allograft
rejection and acute tubular necrosis are the most
important causes of renal allograft dysfunction [2],
and the long-term function of the renal graft and
survival of the patient depend crucially on distin-
guishing these two entities from one another, a task
made more difficult by the possibility of their coex-
istence in the same patient.
Imaging modalities currently used to assess renal
allograft dysfunction include Doppler ultrasound and
renal scintigraphy, neither of which can differentiate
reliably among the medical causes of impaired renal
function [56]. Definitive diagnosis of these condi-
tions often requires a renal biopsy, an invasive
procedure with risks that include hemorrhage, arte-
riovenous fistula, pseudoaneurysm, and infection,
each of which alone can lead to loss of the renal
allograft. The challenge is to find a reliable, non-
invasive, and comprehensive method of examining
the renal allograft and obviate renal biopsy. Early
results with functional MR imaging are promising
and are based on visualizing distinct patterns of
gadolinium enhancement associated with pathologies
that affect different portions of the nephron (Fig. 6).
Szolar et al [2] used MR renography to examine
renal allografts during the posttransplant periods of
23 consecutive patients with clinically suspected
acute allograft rejection or acute tubular necrosis
and demonstrated distinct patterns of cortical and
medullary enhancement in the two groups. Using
Gd-DTPAenhanced GRE images, 12 out of 13 pa-
tients with pure acute tubular necrosis were found to
have a slight decrease and delay in cortical enhance-
ment and a uniphasic instead of biphasic medullary
enhancement pattern when compared with normal
controls. All 10 patients with acute allograft rejection
had significantly decreased cortical and medullary
enhancement when compared with normal controls
and patients with acute tubular necrosis. Four patients
with acute allograft rejection had superimposed acute
tubular necrosis, and MR renography was unable to
distinguish them from those who had acute allograft
rejection alone.
Although less common with newer immunosup-
pressive agents, cyclosporine Atoxicity can also cause
transplant dysfunction. Agildere et al [56] used a turbo
FLASH sequence with 2 mL of Gd-DTPA to obtain
A.J. Huang, V.S. Lee / Radiol Clin N Am 41 (2003) 10011017 1012
cortical and medullary signal intensity curves for
studying the differences between acute allograft rejec-
tion and cyclosporine A toxicity in 17 renal transplant
patients. Although the sample size was small, results
showed abnormally low initial mean signal intensities
and low final mean steady-state signal intensities in
patients with acute allograft rejection compared with
those with cyclosporine A toxicity, likely attributable
to the conspicuous role that decreased cortical perfu-
sion plays in acute allograft rejection.
Functional studies also have proved useful in
diagnosing ureteral complications of renal transplan-
tation. Dorsam et al [57] evaluated the ability of
MR urography to diagnose such complications in
15 patients, 11 of whom had elevated serum creatinine
levels. In six patients whose MR urography exami-
Fig. 6. Renal transplant dysfunction in a 62-year-old man who underwent transplantation 10 weeks earlier. Conventional
contrast-enhanced three-dimensional T1- and T2-weighted imaging of the transplanted kidney showed (A) a patent arterial
anastomosis, (B) a patent venous anastomosis, and (C) a normal collecting system without ureteral obstruction or lymphocele.
Low-dose functional MR renography (dashed line, similar to the technique shown in Fig. 1) using 4-mL Gd-DTPA revealed
(D) normal cortical perfusion, (E) slightly delayed medullary enhancement, and (F) markedly diminished contrast excretion
when compared with MR renography performed 6 days after transplantation when renal function was normal (solid line). This
pattern of enhancement suggests the diagnosis of acute tubular necrosis rather than rejection [2]. This was confirmed by biopsy.
A.J. Huang, V.S. Lee / Radiol Clin N Am 41 (2003) 10011017 1013
nations showed moderate hydronephrosis of the allo-
graft but no obstruction, subsequent clinical follow-up
revealed stable performance of the allograft.
Summary
MR imaging is the only single noninvasive test
that can potentially provide a complete picture of
renal status with minimal risk to the patient, simulta-
neously improving diagnosis while lowering medical
costs by virtue of its being a single test [49]. The
strengths of MR imaging lie in its high spatial and
temporal resolution and its lack of exposure to
ionizing radiation and nephrotoxic contrast agents.
This article reviews the use of MR imaging for
quantification of renal functional parameters and its
application to clinical problems, such as RVD, hydro-
Fig. 6 (continued).
A.J. Huang, V.S. Lee / Radiol Clin N Am 41 (2003) 10011017 1014
nephrosis, and renal transplantation. Although advan-
ces in both the technical and clinical aspects of
functional renal MR imaging have been made, much
remains to be done. The preliminary results reported
in the many studies reviewed are exciting, but these
techniques need to be validated against accepted
standards where such standards exist. In addition,
and perhaps more important, the effects of these new
diagnostic methods on patient outcomes must be
studied. Finally, further progress in image processing
and analysis must be made to make functional renal
MR imaging truly practical. With these advances, one
can expect functional renal MR imaging to play an
ever-expanding and influential role in the care and
management of the patient with renal disease.
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A.J. Huang, V.S. Lee / Radiol Clin N Am 41 (2003) 10011017 1017
Imaging of renal trauma
J. Kevin Smith, PhD, MD
*
, Philip J. Kenney, MD
Department of Diagnostic Radiology, University of Alabama at Birmingham Health System, 619 South 19th Street,
Birmingham, AL 35233, USA
Trauma is nondiscriminatory and affects children,
adolescents, young adults, pregnant women, and the
elderly. Trauma is the second leading cause of years
of life lost for all Americans and the leading cause of
death and disability for youth and young adult
Americans. The financial cost of injuries in America
is estimated at more than $224 billion each year [1].
Despite advances in the technology of motor vehicle
safety, motor vehicle collision remains the most
common cause of blunt abdominal trauma in the
United States. Other less frequent sources of blunt
trauma to the abdomen include falls from a height,
assaults, bicycle accidents, and horseback riding
injuries. Renal injury is the most frequent urologic
trauma and occurs in up to 8% to 10% of patients
with significant blunt or penetrating abdominal trau-
ma; up to 80% of renal injuries are caused by blunt
trauma, mostly motor vehicle accidents, and most
significant renal injuries are associated with other
major organ injuries [2,3].
Care of the traumatized patient requires a multi-
disciplinary approach. The goal of trauma care is to
resuscitate the patient, to diagnose injuries, and to
implement appropriate therapeutic measures as quick-
ly as possible. Radiologists largely play a role in the
diagnosis and staging of injuries. Interventional radi-
ologists play an additional role in the management of
arterial injuries using angiography with transcatheter
embolization. To be an effective member of the
trauma team, the radiologist must be available for
emergent consultation, be adept at the imaging mo-
dalities used in the evaluation of the trauma patient,
and be familiar with those injuries sustained in blunt
abdominal trauma.
Current trends in trauma care are for less invasive
procedures and more conservative management of
many injuries, including renal injuries [2,4,5]. Better
resuscitation techniques, organization of dedicated
trauma centers, and faster response times are chang-
ing the way trauma surgeons evaluate patients. Im-
aging of trauma patients can help to determine which
patients can be managed conservatively and which
patients may require surgery, and to improve long-
term patient outcome.
Selection of patients to image
Most (95%) significant renal injuries are associated
with hematuria, but hematuria may be absent, espe-
cially with renal vascular injuries and ureteropelvic
junction (UPJ) avulsion or ureteral injuries [6,7]. Only
about 1 to 5 out of 1000 blunt trauma patients with only
microscopic hematuria and without hypotension have
significant urinary tract injury [811], so microhema-
turia alone is not an absolute indication for imaging.
At the authors institution abdominal and pelvic CT
is routinely used for blunt trauma patients with
abdominal symptoms, hypotension, or significantly
depressed level of consciousness. CT is used for
evaluation specifically of the genitourinary (GU) tract
for patients with gross hematuria; microscopic hema-
turia and hypotension; or patients with injuries asso-
ciated with renal injuries, such as lumbar spine, lower
rib, or transverse process fractures. Patients with pene-
trating trauma and any degree of hematuria undergo
urologic imaging. CT of all pediatric trauma patients
with any hematuria, even microscopic hematuria
0033-8389/03/$ see front matter D 2003 Elsevier Inc. All rights reserved.
doi:10.1016/S0033-8389(03)00075-7
* Corresponding author. N358 Jefferson Towers, De-
partment of Radiology, University of Alabama Hospital, 619
South 19th Street, Birmingham, AL 352496830.
E-mail address: jksmith@uabmc.edu (J.K. Smith).
Radiol Clin N Am 41 (2003) 10191035
alone, has traditionally been advocated but recent evi-
dence suggests an approach similar to adult trauma pa-
tients may be acceptable [12].
Imaging modalities
Radiography
Radiography is an important tool in the primary
evaluation of chest and skeletal trauma; however, its
use in the setting of blunt abdominal trauma is
virtually nonexistent. Previously described signs of
hemoperitoneum on radiography are not of sufficient
sensitivity or specificity to be useful. The widespread
availability of CT, and to some degree ultrasonogra-
phy (US), has replaced abdominal radiography in this
regard. Radiography does still play a role in the
setting of penetrating trauma to the abdomen.
Intravenous urography
Traditionally, genitourinary injury has been
assessed by intravenous urography (IVU), standard
cystography, and retrograde urethrography. With
ready availability of CT the IVU has taken a more
limited role because of its lower sensitivity for in-
jury, lesser sensitivity for urinary contrast extravasa-
tion, and lack of ability to detect nonurologic injuries
(Fig. 1) [13,14]. The IVU still may be used if CT
is not readily available, for unstable patients going to
surgery, or for urologic imaging if the patient is al-
ready in the operating room. This is typically per-
formed as a one-shot intravenous pyelogram, which
actually consists of a scout radiograph and typically
one film immediately after contrast injection and
another about 10 minutes after contrast injection.
Additional delayed films may be needed if there is
delayed excretion of contrast and to detect urinary
contrast extravasation. The IVP may demonstrate loss
of the renal outline or psoas shadow if there is
perinephric hemorrhage, diminished or nonexcretion
(Fig. 2), or contrast extravasation from an injured
kidney. The ureters should be visualized to evaluate
for ureteral injury or displacement and contralateral
functioning kidney confirmed if there is significant
renal injury, in the event the injured kidney may need
to be removed [5,15].
Fig. 1. (A) Ten-minute radiograph from a one-shot intravenous pyelogram on a patient involved in a motor vehicle collision
shows normal kidneys and ureters bilaterally. (B) Image from contrast CT of the abdomen shows a splenic laceration with active
contrast extravasation (arrow).
J.K. Smith, P.J. Kenney / Radiol Clin N Am 41 (2003) 10191035 1020
Ultrasound
The use of abdominal US in trauma patients
continues to be controversial; the use of US for
detection of renal and urologic injuries is particularly
problematic. US is able to detect free fluid in the
abdomen and pelvis but it cannot distinguish between
extravasated urine, blood, and other types of fluid, an
often clinically important distinction, and cannot
determine the source of bleeding. US is less sensitive
at depicting solid organ injury, especially of the
kidneys, depicting as few as 22% of renal injuries
[16,17]. Although significant renal injuries are often
associated with other abdominal injuries, isolated
renal injuries may not have associated peritoneal fluid
in as many as 65% of the cases (Fig. 3) [16]. In
addition, US is insensitive for retroperitoneal blood
and hollow organ injury [18].
Nevertheless, US has gained moderate acceptance
in the United States as a means to evaluate the patient
with blunt abdominal trauma. US in the setting of
trauma usually consists of a focused abdominal
sonography for trauma (FAST) scan. FAST scans
can be completed in several minutes during the
resuscitation of the patient in the trauma bay. The
primary goal of the FAST scan is the identification of
free fluid (hemoperitoneum) in the unstable patient, a
finding that usually prompts an exploratory laparot-
omy. The FAST scan usually consists of interrogation
of six locations for the presence of free fluid: (1) the
right upper quadrant including the hepatorenal recess,
(2) the left upper quadrant including the splenorenal
recess, (3 and 4) both paracolic gutters, (5) the pelvis
including its various peritoneal cavity recesses, and
(6) the pericardial space [19].
Various studies have proposed using US to search
for solid organ injury, but sufficient sensitivities and
specificities have not been demonstrated [2022].
US has also been used to screen all blunt abdominal
trauma victims as part of a management algorithm. In
some institutions, radiologists or sonologists perform
the US examination, but in many centers this task
falls to the trauma surgeon or emergency physician.
There is little satisfactory training for clinical US in
these specialties and virtually no training in the
technical aspects of US; the ability of such individ-
uals to perform quality examinations has been seri-
ously questioned. If trauma US is to be performed by
the radiology department, the service must be readily
available at all times.
Ultrasound may show renal laceration or a change
in echogenicity of the injured kidney, or a decrease in
the usual perinephric echogenicity if there is peri-
nephric fluid or hemorrhage. If US is negative and
there is significant hematuria, or if the US is positive,
CT is still indicated for better evaluation of the injury
if the patient is stable. For this reason the use of US is
probably best reserved for rapid evaluation for intra-
peritoneal fluid in the unstable patient who may
require urgent surgery.
Angiography
Before the widespread availability of CT, angiog-
raphy was often used to evaluate renal abnormalities
seen at IVU, especially suspected arterial injuries.
With the advent of faster CT scanners and their
increased detection of active arterial extravasation,
angiography is being used less frequently for the
initial diagnosis of traumatic injuries. CT shows
many injuries not seen at angiography and accurately
characterizes most vascular injuries. Even vascular
contrast extravasation is better depicted by CT. Con-
versely, the role of angiography in the management of
vascular and exsanguinating solid-organ injuries con-
tinues to increase given the emphasis on nonoperative
management of trauma patients. Angiography with
transcatheter embolization is becoming the standard
of care in the treatment of patients with many
vascular injuries. Angiographic embolization is well-
suited to treat traumatic pseudoaneurysms and active
arterial bleeding caused by splenic or hepatic and
sometimes renal injury, and hemorrhage associated
with pelvic ring injury [2325].
Fig. 2. Absent nephrogram. Ten-minute radiograph from a
one-shot intravenous pyelogram of a patient involved in a
motor vehicle collision shows no enhancement or contrast
excretion on the right.
J.K. Smith, P.J. Kenney / Radiol Clin N Am 41 (2003) 10191035 1021
Diagnostic peritoneal lavage
The diagnostic peritoneal lavage is not an imag-
ing modality but is the traditional gold standard for
evaluating for abdominal injury, and is safe and
rapid when performed by experienced surgeons.
Early studies showed diagnostic peritoneal lavage
to be faster and more rapid than CT, and many
showed diagnostic peritoneal lavage to have better
accuracy [2629]. With improvements in CT tech-
niques including dynamic and then helical scanning,
increased experience with CT, and location of CT in
close physical proximity to the trauma bay, however,
these differences have been erased [30]. For renal
injuries diagnostic peritoneal lavage, like ultrasound,
may be especially problematic because isolated renal
injuries may not be associated with intraperitoneal
fluid, and when positive the diagnostic peritoneal
lavage is not specific for the type of injury. Some
authors argue screening diagnostic peritoneal lavage
with selective use of CT is less expensive, but actual
cost analysis is lacking [31]. At the authors institu-
tion, there is a multidetector CT scanner in the emer-
gency department within a few feet of the trauma
bay and diagnostic peritoneal lavage is now infre-
quently performed.
Retrograde pyelography
Retrograde pyelography is primarily useful if
ureteral, UPJ, or renal pelvic injury is suspected
and delayed images were not obtained or were not
adequate to exclude these injuries on CT or IVU. It
is often not practical in the emergent evaluation of
the severely injured patient, however, and does not
characterize renal parenchymal injuries.
Fig. 3. Trauma ultrasound. (A) Ultrasound gray-scale image of a patient involved in a motor vehicle collision shows normal
right kidney. (B) Ultrasound image with power Doppler shows no blood flow within the right kidney. (C) Contrast-enhanced CT
image shows nonenhancing right kidney. Note relatively small amount of hemorrhage and the blind ending stump of the renal
artery (arrow).
J.K. Smith, P.J. Kenney / Radiol Clin N Am 41 (2003) 10191035 1022
Radionuclide renal scintigraphy
Radionuclide renal scintigraphy may be used to
evaluate the renal function of injured kidneys, eval-
uate perfusion of a kidney with demonstrated or
suspected arterial injury, and for evaluation of the
repaired kidney or renal vasculature. Since the wide-
spread availability of CT, renal scintigraphy is rarely
used in the acute setting.
MR imaging
MR imaging with gadolinium may be helpful to
assess or characterize renal injury in the stable patient
with strong contraindication for iodinated contrast,
but MR imaging is usually not practical in the acutely
severely injured patient because of motion artifacts
and the time often required.
CT
CT is the most comprehensive diagnostic tool
available for the evaluation of the victim of blunt
abdominal trauma. Unlike US and diagnostic perito-
neal lavage, which are limited to answering certain
specific diagnostic questions (eg, is there hemo-
peritoneum), CT affords a comprehensive evaluation
of all the intra-abdominal structures. One of the major
advantages of CT is its ability to stage injuries to the
abdomen. The trend toward greater nonoperative
management of traumatic abdominal injuries can be
attributed in large part to successful staging of inju-
ries by CT. It is desirable to have the CT scanner as
close to the trauma bay as possible to minimize pa-
tient transport time.
CT technique
Optimal evaluation of the blunt abdominal trauma
victim requires optimization of CT technique. Ade-
quate scans can be obtained on conventional axial CT
scanners, but helical CT scanners offer a substantial
gain in speed and quality. Multidetector CT scanners
have given the trauma radiologist an even more
powerful tool compared with single-slice helical CT.
Thin-section, high-quality images can be obtained in
a fraction of the time required for even helical single-
slice scanners. Shorter scan times mean less time for
motion and breathing artifact. Multidetector CT
allows for optimal detection of injuries, such as active
arterial contrast extravasation, while decreasing the
time that critically injured trauma patients are re-
quired to be in the CT scanner. Multidetector CT is
not only faster but also offers much more efficient use
of tube-heat capacity so that multiple, consecutive CT
examinations can be performed without having to
wait for the CT tube to cool.
Intravenous contrast is a necessity for satisfactory
accuracy in abdominal CT scans performed for trau-
ma. Solid organ injuries, such as liver, splenic, or
renal lacerations, can be unapparent on noncontrast
scans. Active arterial extravasation can only be
detected with the use of intravenous contrast. Low-
osmolality, nonionic contrast is preferred. A typical
contrast dose is 120 to 150 mL for adults and 1.5 to
2 mL/kg for children. An injection rate of at least
2 mL/second is desirable, but rates in the range of 3 to
4 mL/second provide optimal vascular and parenchy-
mal enhancement. Helical CT and multidetector
CT scanners have increased the frequency with which
active arterial extravasation can be detected.
Most authors favor the use of oral contrast in
trauma abdominal CT scans. Oral contrast is safe,
even in children [32,33]. Administration of oral
contrast can aid greatly in the detection of bowel
injuries. A dilute solution of 4% diatrizoate meglu-
mine in tap water is administered by mouth or by
nasogastric tube as soon as the abdominal CT is
requested. A volume of 400 to 600 mL is given.
For trauma patients the scan is not delayed for
passage of oral contrast through the bowel. In this
short time frame, usually only the stomach, duode-
num, and proximal jejunum are opacified. Fortunate-
ly, these are some of the most common sites of bowel
injury. Some authors suggest withdrawing the naso-
gastric tube into the distal esophagus during the scan
to reduce streak artifact in the upper abdomen.
Five millimeters or less image thickness is helpful
to avoid significant volume averaging artifacts. For
single-slice helical CT a scanner pitch of 1.5:1 is a
good compromise between speed and excessive slice
profile broadening. On a multidetector CT scanner
high-speed (pitch greater than one) scanning speeds
the image acquisition and still generally results in
excellent image quality. It may be helpful to scan at
less than the maximum table speed to allow retro-
spective reconstruction of thinner slices if needed for
subtle injuries or the evaluation of associated spine or
bony pelvic injuries. For example, on a General
Electric four-slice scanner the authors use HS mode
with 5-mm images and table speed of 15 mm per
rotation, 0.8-second scanning. This allows retrospec-
tive reconstruction of 2.5-mm thick slices if needed.
With the newer 16 or more slice scanners even the
fastest table speeds still allow reconstruction of very
thin slices if needed. Kilovolt (peak) is usually 140
and milliampere seconds between 100 and 300 de-
pending on scan mode and patient size. The acquisi-
tion start times after beginning contrast injections are
J.K. Smith, P.J. Kenney / Radiol Clin N Am 41 (2003) 10191035 1023
45 seconds for chest and 75 seconds for abdomen; a
pause of 180 seconds before scanning the pelvis al-
lows the bladder to opacify if a CT cystogram is not
going to be performed. Some centers routinely scan
through the kidneys a second time during the uro-
graphic phase of enhancement to detect subtle paren-
chymal and collecting system injuries. The authors
trauma patients images are routinely evaluated as
they are obtained while the patient is still on the CT
scanner and if there is significant perinephric or peri-
ureteral fluid, delayed images (10 to 15 minutes) are
obtained to evaluate for urinary contrast extravasation
Standard CT with intravenous contrast has been
shown to yield up to 40% false-negatives for bladder
injury. If bladder injury is a clinical concern (gross
hematuria or pelvic ring fracture), a cystogram or CT
cystogram should be performed. After the initial scan,
the patient can be evaluated by CT cystography
without having to move to another location. CT cys-
tography is equal to or better than conventional cys-
tography if adequate retrograde bladder distention is
achieved with dilute contrast and CT cystography is
capable of distinguishing intraperitoneal, extraperito-
Fig. 4. Renal contusion. Contrast-enhanced CT of a patient
in a motor vehicle collision with small, ill-defined wedge-
shaped area of slight hypoenhancement in the mid right
kidney (arrow).
Fig. 5. Subcapsular hematoma. Contrast-enhanced CTscan of
a patient involved in a motor vehicle collision demonstrates a
crescentic high-density fluid collection around the left kidney
(arrows). Note the relatively well-defined outer margin and
the deformity of the underlying renal parenchyma.
Fig. 6. Perinephric and subcapsular hematomas. Contrast-
enhanced CT scan of a patient involved in a motor vehicle
collision shows an ill-defined high-density fluid collection
in the perinephric space (arrows). This patient also had a
subcapsular hematoma with deformity of the renal paren-
chyma (arrowheads).
Fig. 7. Grade 23 renal injury: renal laceration. Contrast-
enhanced CT scan of a patient involved in a motor vehicle
collision shows slightly irregular low-attenuation defect in
the anterior left kidney with associated perinephric fluid.
J.K. Smith, P.J. Kenney / Radiol Clin N Am 41 (2003) 10191035 1024
neal, or combined bladder rupture [34]. For CT
cystography, once the abdominal CT scan is com-
plete, the urinary bladder is drained by Foley catheter.
The bladder is then filled by gravity infusion with
dilute iodine-based contrast (12 mL of 300-strength
contrast in 500 mL normal saline) and the pelvis
scanned again when the bladder is fully distended
taking care to include the entire urinary bladder.
Trauma patients with histories consistent with
urethral trauma, gross blood at the urethral meatus,
or high-riding prostate gland on physical examination
should undergo a retrograde urethrogram before
placement of a Foley catheter. Patients with a lower
index of suspicion can undergo a pericatheter urethro-
gram at a later time and a catheter is generally placed
during the initial assessment in the trauma bay.
CT interpretation
Thoroughness and attention to detail are of vital
importance in the interpretation of CT scans for blunt
Fig. 8. Grade 3 renal injury: renal laceration. (A) Contrast-enhanced portal venous phase image froma CTscan of a patient involved
in a motor vehicle collision has an irregular nonenhancing renal parenchymal defect in the mid lateral left kidney with associated
perinephric hematoma. (B) Delayed image from the same CT scan shows no urinary contrast extravasation.
Fig. 9. Grade 4 renal injury: renal laceration into collecting system. (A) Tiny amount of fluid medial to the renal pelvis (arrow)
was the only clue to this laceration involving the collecting system. (B) Delayed image from the same CT shows a tiny area of
urinary contrast extravasation (arrow).
J.K. Smith, P.J. Kenney / Radiol Clin N Am 41 (2003) 10191035 1025
abdominal trauma. A complete evaluation of a trauma
CT involves viewing the entire scan with three dif-
ferent window-level settings: (1) soft tissue, (2) lung,
and (3) bone. Immediate life-threatening injuries
should be sought first: large hemoperitoneum, large
or tension pneumothorax, pneumoperitoneum, signs
of hypovolemic shock, and active arterial extravasa-
tion. Each area of the abdomen and pelvis should
then be interrogated for the presence of injury: liver
and right paracolic gutter; spleen and left paracolic
gutter; upper abdominal organs including the stom-
ach, duodenum, pancreas, gallbladder, and biliary
tree; retroperitoneum including the adrenals, kidneys,
inferior vena cava, and aorta; small bowel, colon, and
mesentery; pelvis including the urinary bladder;
muscles including the abdominal wall, psoas, iliacus,
and gluteals; bones including the spine and pelvis;
and thighs (looking for soft tissue hematoma). West
[35] describes this systematic review as the every-
organ-on-every-slice approach. The authors believe
image review on the modern PACs workstation is
best done by paging relatively rapidly through the
images multiple times, paying specific attention to a
specific organ during each pass through the images.
The authors prefer to describe this approach for
image review as every-slice-of-every-organ.
Classification of renal injuries
Renal injuries are graded by the American Asso-
ciation for the Surgery of Trauma according to the
Fig. 10. Grade 4 renal injury: lacerations extending into the collecting system. (A) Contrast-enhanced CT scan of a patient
involved in a motor vehicle collision shows several deep lacerations into the collecting system (arrows). (B) Delayed image from
the same CT scan shows urinary contrast extravasation (arrow).
Fig. 11. Grade 4 renal injury: segmental infarctions. (A) Contrast-enhanced CT scan of a patient involved in a motor vehicle
collision shows well-defined, wedge-shaped, nonenhancing areas in the mid left kidney. (B) Follow-up contrast-enhanced CTscan
of the same patient shows complete resolution of the findings in about 2 weeks.
J.K. Smith, P.J. Kenney / Radiol Clin N Am 41 (2003) 10191035 1026
depth of the injury and involvement of vessels or the
collecting system as follows[36]:
Grade 1
Hematuria with normal imaging studies
Contusions
Nonexpanding subcapsular hematomas
Grade 2
Nonexpanding perinephric hematomas con-
fined to the retroperitoneum
Superficial cortical lacerations less than 1 cm
in depth without collecting system injury
Grade 3
Renal lacerations greater than 1 cm in depth
that do not involve the collecting system
Grade 4
Renal lacerations extending through the kid-
ney into the collecting system
Injuries involving the main renal artery or vein
with contained hemorrhage
Segmental infarctions without associated lac-
erations
Grade 5
Shattered or devascularized kidney
UPJ avulsions
Complete laceration or thrombus of the main
renal artery or vein
These scores were devised principally to facilitate
clinical research, but the radiologist should be familiar
with the scoring system because it is part of the
language of evaluation and triage use by the trauma
surgeon. In general the American Association for
the Surgery of Trauma injury grade correlates with
the perceived need for surgery to repair or remove the
injured kidney [37]. Even with high-grade injuries,
Fig. 12. Grade 4 renal injury: infarctions and associated
laceration. Contrast-enhanced CT scan of a patient involved
in a motor vehicle collision shows well-circumscribed,
wedge-shaped areas of nonenhancement posteromedially in
both kidneys (arrows). The right kidney has associated
laceration and hematoma. Note also the peritoneal fluid and
bowel edema (shock bowel).
Fig. 13. Grade 5 renal injury: infarctions and multiple deep lacerations. (A) Contrast-enhanced CT scan of a patient involved in a
motor vehicle collision shows a well-defined, wedge-shaped, nonenhancing infarction (arrow) and several deep, irregular,
nonenhancing lacerations. (B) Delayed image from the same CT scan has contrast extravasating medially and laterally from the
deep lacerations.
J.K. Smith, P.J. Kenney / Radiol Clin N Am 41 (2003) 10191035 1027
however, nonoperative management may be success-
ful or even preferred in stable patients because renal
function is often better preserved with nonoperative
management [5,38]. Unless there is extensive devital-
ized tissue, active hemorrhage, a large injury to the
collecting system, or ureteral disruption, renal injuries
are often managed conservatively [39,40].
Grade 1 injuries
American Association for the Surgery of Trauma
grade 1 renal injuries account for about 80% of renal
injuries and include hematuria with normal imaging
studies, contusions, and nonexpanding subcapsular
hematomas. Contusions are seen as either ill-defined
Fig. 14. Grade 5 renal injuries: shattered kidney with venous injury managed conservatively. (A) Contrast-enhanced CTscan of a
patient involved in a motor vehicle collision demonstrates nearly occlusive thrombus in the right renal vein (arrow). (B) A slightly
lower image from the same CT scan has multiple deep, irregular hypodense lacerations extending through the renal parenchyma
with hematoma within the lacerations and around the kidney and devitalized segments of renal parenchyma (arrow). (C) Delayed
image fromthe same CTscan shows faint residual area of vascular contrast extravasation (arrow), which is much less dense than the
adjacent ureteral contrast. (D) Follow-up contrast-enhanced CTscan on the same patient. The kidney is deformed but the renal vein
injury and the urinary leak resolved and there is considerable residual functioning renal parenchyma.
J.K. Smith, P.J. Kenney / Radiol Clin N Am 41 (2003) 10191035 1028
or sometimes sharply marginated areas of decreased
enhancement and excretion. They are distinguishable
from segmental infarctions by the presence of en-
hancement (Fig. 4). Subcapsular hematomas are less
common in blunt trauma than perinephric hematomas
and show up as an often high-density fluid collection
contained between the renal parenchyma and the
renal capsule, frequently with some deformity of
the underlying kidney. When small they may be
crescentic (Fig. 5), but larger collections may become
elliptical and compress the renal parenchyma (Fig. 6).
Rarely, the collection may compress the kidney
enough to decrease the renal perfusion and result in
reactive hypertension, the so-called Page kidney.
Grade 2 and 3 injuries
Grade 2 injuries include nonexpanding perinephric
hematomas confined to the retroperitoneum and
superficial cortical lacerations less than 1 cm in depth
without collecting system injury. The perinephric
hematoma may be an isolated injury but is often
associated with underlying renal injury. It manifests
on CT as a typically ill-defined, often high-density
fluid collection between the renal parenchyma and
Gerotas fascia (see Fig. 6). The presence of a peri-
nephric hematoma should prompt a thorough search
for an underlying renal injury. A perinephric hema-
toma may be quite large, but traditionally does not
deform the kidney as opposed to the typical sub-
capsular hematoma, which often does deformthe renal
contour when large.
Renal lacerations appear as irregular or linear
parenchymal defects, which may contain blood or
clot, and may be higher than water density but are
without enhancement. Grade 2 lacerations are defined
as less than 1 cm in depth and without involvement of
the collecting system (Fig. 7), and have no urinary
contrast extravasation. Grade 3 renal injuries include
similar renal lacerations that are greater than 1 cm,
but do not involve the collecting system (Fig. 8).
Grade 1 to 3 renal injuries are almost always man-
aged conservatively unless there is brisk active hem-
orrhage [39,40]. Active hemorrhage may be managed
successfully with selective catheter embolization if
the patient is otherwise stable [41,42].
Grade 4 injuries
Renal lacerations extending through the kidney
into the collecting system or injuries involving the
main renal artery or vein with contained hemorrhage
are classified as grade 4. Lacerations involving the
collecting system frequently lead to extravasation of
urine and urinary contrast; any time there are lacer-
ations extending through the kidney or significant
perinephric fluid, especially around the renal hilum,
delayed images should be obtained to evaluate for
urine extravasation (Figs. 9, 10). Even large urinary
extravasations often resolve with conservative treat-
ment, but stenting may be helpful with larger leaks. If
there is significant devitalized renal tissue, especially
with concomitant intraperitoneal injuries, in addition
to the urine leak, surgical debridement or repair may
be needed to prevent later development of urinoma
and infection or abscess formation, which may ne-
cessitate nephrectomy to prevent sepsis [4].
Fig. 15. Grade 5 renal injury: ureteropelvic junction avulsion. (A) Five-minute film from an intravenous pyelogram on a patient
involved in a motor vehicle collision shows relatively minor calyceal blunting on the left. (B) Ten-minute film shows progressive
accumulation of urinary contrast adjacent to the blind ending proximal ureter. The lack of contrast in the more distal ureter
suggests a complete tear.
J.K. Smith, P.J. Kenney / Radiol Clin N Am 41 (2003) 10191035 1029
Segmental infarctions without associated lacera-
tions are also grade 4 injuries. Segmental infarctions
may occur because of thrombosis, dissection, or lac-
eration of segmental arteries and are often associated
with other renal injuries. They manifest as well-
circumscribed, linear or wedge-shaped, often multi-
focal nonenhancing areas extending through the renal
parenchyma in a radial or segmental orientation
(Figs. 11, 12). They usually resolve spontaneously
(see Fig. 11) or result in relatively minor renal scaring
and are treated conservatively [43,44]. Rarely hyper-
tension may develop as a delayed complication in
6% to 20% of patients but often resolves or can be
medically managed [25,45].
Grade 5 injuries
Injuries resulting in a shattered or devascularized
kidney, UPJ avulsions, and complete laceration or
thrombosis of the main renal artery or vein are
classified as grade 5 renal injuries. A shattered kidney
is basically the extreme of multiple renal lacerations,
Fig. 16. Grade 5 renal injury: ureteropelvic junction avulsion. (A) Contrast-enhanced CT of a patient involved in a motor vehicle
collision has a small amount of medial perinephric fluid (arrows). (B) Delayed image from the same CT scan shows medial
perinephric urinary contrast extravasation and no contrast in the more distal ureter.
Fig. 17. Grade 5 renal injury: ureteropelvic junction avulsion. (A) Contrast-enhanced CT of a patient involved in a motor vehicle
collision has a moderate perinephric fluid collection (straight arrows) and minimal medial perinephric fluid (white arrow).
(B) Delayed images of the same CT scan demonstrate urinary contrast extravasation and lack of opacification of the distal ureter.
J.K. Smith, P.J. Kenney / Radiol Clin N Am 41 (2003) 10191035 1030
and there are often devitalized areas caused by
concomitant infarction, and urinary extravasation
caused by associated injuries to the collecting system
(Figs. 13, 14).
Injury of the UPJ occurs because of shearing
stress at the renal pelvis; during rapid deceleration
or hyperextension the kidney pulls on the relatively
fixed ureter and renal artery and vein. The UPJ injury
may be complete avulsion or partial tear. Both ex-
hibit characteristic medial or circumrenal urinoma
(Figs. 1517) [4648]. The partial tear may be dis-
tinguished from the complete avulsion by the pres-
ence of contrast in the distal ureter [47]. Hematuria is
often absent [47,49]. Complete tears require surgical
Fig. 18. Grade 5 renal injury: missed ureteropelvic junction avulsion. (A) Contrast-enhanced CT on a patient after motor vehicle
collision shows a small amount of medial perinephric fluid (arrows). The significance of the finding was not appreciated, so
delayed images were not obtained. (B) Follow-up contrast-enhanced CT scan of the same patient shows interval development of
hydronephrosis and a large urinoma (arrows). (C) Percutaneous nephrostogram on the same patient shows interruption of the
ureter at or just below the ureteropelvic junction with extravasation of urinary contrast and no filling of the distal ureter. A
nephrectomy was eventually performed because of infection of the urinoma.
J.K. Smith, P.J. Kenney / Radiol Clin N Am 41 (2003) 10191035 1031
repair, but some partial tears may resolve with stent-
ing or observation. If the diagnosis is missed and the
proximal collecting system is not drained, urinoma
may form and nephrectomy may be needed (Fig. 18).
A devascularized kidney most commonly results
from an incomplete vascular tear with thrombosis
involving the main renal artery. Hematuria is often
absent, especially if there are not other associated
injuries [50]. The kidney is nonenhancing, and there
may be little hematoma or other sign of injury (see
Fig. 3; Fig. 19). The blind ending renal artery is
sometimes seen and there may be retrograde opacifi-
cation of the renal vein or cortical rim sign, which may
not be apparent early [51]. More rarely, there is
complete tear of the artery with massive hematoma
or active bleeding. These injuries are often associated
with other renal injuries and this contributes to poor
renal outcome of attempted repair so the management
is usually expectant for stable patients or nephrectomy
if there is active bleed or major parenchymal disrup-
tion, unless there is injury or absence of the contralat-
eral kidney [50,52]. Hypertension may develop as a
delayed complication weeks to months after the injury
in as many as 40% to 50% of patients; often the
hypertension resolves or can be managed medically
but occasionally nephrectomy is required [50,52].
Injuries to the main renal vein are another less
common form of vascular pedicle injury. There may
be thrombosis with CT typically showing filling
defect (see Fig. 14A) or nonenhancement of the vein
and delayed or persistent nephrogram with complete
occlusion [46,53]. Laceration of the renal vein
presents with medial or circumrenal subcapsular or
perinephric hematoma.
Vascular contrast extravasation
Bright enhancement close to the density of nearby
arteries within a laceration or around an injured
kidney during the early phases of CT scanning
indicates either contained or active hemorrhage. A
contained hemorrhage or pseudoaneurysm is fairly
well circumscribed and contained within the renal
Fig. 19. Grade 5 renal injury: main renal artery. Contrast-
enhanced CT on a patient in a motor vehicle collision with
nonenhancing right kidney. Note the relative lack of peri-
nephric fluid. There was no hematoma.
Fig. 20. Active vascular contrast extravasation. Contrast-
enhanced CT on a patient in a motor vehicle collision with a
tiny renal laceration, but with large subcapsular and peri-
nephric hematomas and waterfall- shaped extravasation of
vascular contrast into the hematoma (arrow).
Fig. 21. Active vascular contrast extravasation. Contrast-
enhanced CT on a patient in a motor vehicle collision with a
small renal laceration, but with large subcapsular and peri-
nephric hematomas and flame-shaped extravasation of vas-
cular contrast into the hematoma (arrow).
J.K. Smith, P.J. Kenney / Radiol Clin N Am 41 (2003) 10191035 1032
parenchyma or laceration. Active hemorrhage is ill-
defined or flame- or waterfall-shaped, with an asso-
ciated fresh hematoma, which often shows dependant
or circumferential layering of older and fresher hem-
orrhage (Figs. 20, 21). As with other organs, active
extravasation of arterial contrast from the main renal
artery or lacerated kidney may indicate the need for
urgent surgery or transcatheter embolization to pre-
vent exsanguination [5458].
Pseudoaneurysms may persist or enlarge and may
occasionally cause delayed bleeding or rarely hyper-
tension. Arteriovenous fistulas associated with renal
lacerations from blunt or especially penetrating trau-
ma may be unapparent initially but may enlarge over
time, also potentially causing delayed bleeding, hy-
pertension, or high-output cardiac failure.
Summary
Trauma is a major cause of death and disability
and renal injuries occur in up to 10% of patients
with significant blunt abdominal trauma. Patients
with penetrating trauma and hematuria, blunt trau-
ma with shock and hematuria, or gross hematuria
warrant imaging of the urinary tract specifically and
CT is the preferred modality. If there is significant
perinephric fluid, especially medially, or deep lacer-
ation, delayed images should be obtained to evaluate
for urinary extravasation. Most renal injuries are
minor, including contusions, subcapsular and peri-
nephric hematoma, and superficial lacerations. More
significant injuries include deep lacerations, shattered
kidney, active hemorrhage, infarctions, and vascular
pedicle and UPJ injuries. These injuries are more
likely to need surgery or have delayed complications
but may still often be managed conservatively. The
presence of urinary extravasation and large devi-
talized areas of renal parenchyma, especially with
associated injuries of intraperitoneal organs, is par-
ticularly prone to complication and usually requires
surgery. Active hemorrhage should be recognized
because it often indicates a need for urgent surgery
or embolization to prevent exsanguination.
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Imaging of hereditary renal cancer
Peter L. Choyke, MD
Department of Radiology, Imaging Sciences Program, National Institutes of Health, NIH Building 10, Room 1C660,
Bethesda, MD 208921182, USA
Renal cancer is diagnosed in over 30,000 Ameri-
cans each year and accounts for approximately
12,000 annual deaths. Smoking, obesity, and occu-
pational exposures have been implicated in the
development of renal cancers but, in general, the
cause of renal cancer remains obscure [1]. Although
hereditary renal cancer makes up only approximately
4% of the total number of cases, this number is
expected to grow as a more complete understanding
of the genetic causes of cancer is elucidated [2]. As
hereditary renal cancer syndromes become better
understood, they provide insights into the mecha-
nisms of cancer development in the general popula-
tion and assist efforts to prevent and treat renal
cancers (Table 1).
The most common cell type of renal cancer is the
clear cell carcinoma, followed by papillary (types I
and II), chromophobe carcinoma and oncocytoma
[3,4]. Medullary carcinoma and duct of Bellini can-
cers are rare renal tumors. Over the past 5 years,
hereditary renal cancer syndromes have been asso-
ciated with one or more of these cancer cell types.
The genes responsible for these syndromes have been
discovered in many cases and research is now under-
way to explain the molecular pathways leading to
tumor development. A more complete picture of the
mechanisms underlying the development of tumors of
varying cell types is emerging.
Over the past decade substantial progress has been
made in the understanding of the genetic basis of
cancer in humans. This article reviews the current
state-of-the-science of hereditary renal cancers with
particular attention to their imaging features and
clinical management.
Histologic subtypes of renal cancer
Before considering the individual hereditary renal
cancer syndromes it is important to review the char-
acteristics of the different cell types of renal cancer.
Renal cancers can be subclassified into a variety of cell
types (Fig. 1) [5]. Clear cell carcinomas are the most
frequent type of renal cancer accounting for approxi-
mately 75% of renal cancers. The term clear cell
carcinoma encompasses the clear cell variant, the
granular cell variant, and mixed cell types. The high
glycogen content within the cytoplasm of clear cell
cancer cells accounts for their lucent appearance on
conventional histologic stains. When glycogen is less
abundant, the cytoplasm is darker and the cells are
termed granular. A delicate but rich and permeable
vascular supply is often seen throughout these tumors,
although regions of necrosis, fibrosis, or hemorrhage
are avascular or hypovascular. Clear cell carcinomas
are thought to arise from the proximal tubular epithe-
lium of the kidney
The second leading type of renal cancer is termed
papillary, also sometimes called chromophil
renal cancer, which accounts for 10% to 15% of
all renal cancers. There are two subtypes of papillary
renal cell carcinomas, type I and type II, which are
distinguished by tumor architecture and cellular
morphology. Both types share a common papillary
structure: a fibrovascular core with tumor cells lining
the surface of each papilla (see Fig. 1) [5,6]. Type I,
or basophilic renal cancer, usually is considered
clinically low grade and has a favorable prognosis.
This tumor is composed of fronds of fibrovascular
papillary and tubular structures covered by cells with
scanty cytoplasm and small oval nuclei. Foamy
macrophages, which are thought to represent a host
immune response, are often present within the inter-
0033-8389/03/$ see front matter D 2003 Elsevier Inc. All rights reserved.
doi:10.1016/S0033-8389(03)00068-X
E-mail address: pchoyke@nih.gov
Radiol Clin N Am 41 (2003) 10371051
Table 1
The hereditary renal cancers in adults
Syndrome
Genes gene name
(gene Product)
Frequency of
renal cancer (%)
Predominant renal
tumor cell type
Other renal
tumor cell types Associated abnormalities
von-Hippel Lindau 3p26 VHL (pVHL) 2845 Clear cell Cysts CNS hemangioblastomas, retinal
angiomas, pancreatic cysts,
neuroendocrine tumors of pancreas,
pheochromocytoma
Tuberous sclerosis 9q34 TSC1 (hamartin) 16p13
TSC2 (tuberin)
12 Clear cell Cysts, angiomyolipoma,
papillary, chromophobe,
oncocytoma
CNS tubers, angiofibromas of skin,
cardiac rhadomyomas
Hereditary papillary
renal cancer
7q34 c-MET (HGF receptor) 19 Papillary type1 None
Hereditary leiomyoma
renal cell carcinoma
1q42-43 FH (fumarate hydratase) 1530 Papillary type 2 None Cutaneous and uterine leiomyomas
Birt-Hogg-Dube` 17p11.2 BHD (folliculin) 815 Chromophobe
oncocytic neoplasm
Clear cell,
papillary, oncocytoma
Fibrofolliculomas, lung cysts,
pneumothoraces
Familial renal oncocytoma Unknown Unknown Oncocytoma None Renal dysfunction
Medullary carcinoma
of the kidney
11p Unknown Medullary carcinoma None Sickle cell trait
P
.
L
.
C
h
o
y
k
e
/
R
a
d
i
o
l
C
l
i
n
N
A
m
4
1
(
2
0
0
3
)
1
0
3
7
1
0
5
1
1
0
3
8
stitium and psamma bodies also are frequently
present. Despite the apparent vascularity on his-
tology, type I papillary renal tumors typically enhance
poorly on CT or during renal angiography. Type II
papillary tumors, or eosinophilic renal cancers, bear a
superficial resemblance to type I tumors in that the
basic frond-like architecture is present but they may
not be related at a biologic level. Type II papillary
renal cancers consist of papillae covered by large
cells with abundant eosinophilic cytoplasm and large
nuclei with prominent nucleoli. Type II papillary
tumors often are more clinically aggressive than type
I papillary tumors and can enhance more intensely.
Papillary tumors also are thought to arise from the
proximal tubular epithelium
The chromophobe carcinoma, so-named because
of its lack of staining with typical histologic stains,
such as hematoxylin and eosin, is the third most
common type of renal cancer accounting for about
5% of renal tumors. Chromophobe carcinoma can be
stained with Hales colloidal iron, which yields a
homogeneous blue cytoplasmic stain [7]. In routine
histologic sections the cytoplasm tends to condense
near the cell membrane producing a halo around the
nucleus. The cytoplasm is rich in mitochondria
much like the oncocytoma [8]. The oncocytoma
itself is considered a benign renal neoplasm; how-
ever, this categorization has been called into
question by the resemblance of oncocytoma to chro-
mophobe carcinoma and by reports of metasta-
sizing oncocytomas [911]. Oncocytomas are
comprised of cells with abundant eosinophilic cyto-
plasm that are filled with mitochondria accounting
for the brown color on gross pathology. When they
are numerous the term oncocytosis is used and
can be seen in patients with chromophobe carcino-
mas [11]. Chromophobe carcinomas and oncocyto-
mas are thought to arise from intercalated cells in
the distal tubules.
Collecting duct carcinoma includes the medullary
renal cancer associated with sickle cell trait and duct
of Bellini tumors. Medullary renal cancer is charac-
terized histologically by irregular channels lined by
highly atypical epithelium that sometimes have a
hobnail appearance. The channels are found in an
inflamed desmoplastic stroma. [12,13]. Both medul-
lary renal cancer and duct of Bellini tumors are
clinically aggressive neoplasms. Medullary renal can-
cer and its variants arise from the collecting ducts,
which are histologically and embryologically distinct
from the tubular epithelium.
In the following sections the relationship between
each of the preceding cell types of renal cancer and its
corresponding genetic syndrome are described.
Von Hippel-Lindau disease
Von Hippel-Lindau disease (VHL) is a multisys-
tem autosomal-dominant hereditary disorder charac-
terized by the formation of hemangioblastomas in
the spine and posterior fossa, retinal angiomas,
pheochromocytomas, pancreatic cysts, cystadenomas
and neuroendocrine tumors, epididymal and broad
ligament cystadenomas, and renal cysts and tumors.
VHL gives rise to a variety of renal cystic lesions
ranging from pure cysts to mixed solid and cystic
masses to purely solid clear cell carcinomas of the
kidney. The VHL gene, found at 3p25, is considered
an important housekeeping or tumor suppressor gene
that in its normal state functions to prevent the
development of renal cancers. Mutations or inactiva-
tion of the VHL gene are found in over 60% of
sporadic clear cell renal carcinomas indicating that it
is one of the crucial genes in the development of clear
cell carcinoma of the kidney [14,15].
A tumor suppressor gene normally functions to
decrease the chance of developing cancer. When a
tumor suppressor gene is mutated and the resulting
protein product is abnormal, however, the affected
cells are at increased risk of malignancy. Tumor
development requires that both copies of the gene
become mutated or deleted. Unlike other diseases in
which more than one genetic locus has been impli-
cated, VHL seems to be caused by mutations at a
single gene locus, 3p25 (short arm of third chromo-
some). The gene was first discovered in 1993 by Latif
et al [16]. Subsequently it has been demonstrated that
the VHL gene codes for a protein, pVHL. One of the
normal roles of pVHL is to assist in the degradation of
an intracellular growth factor known as hypoxia
inducible factor (HIF) [17]. HIF is an important
regulator of metabolism and is dependent on the
oxygen tension within a cell. Normally, HIF is pro-
duced when the cell is exposed to hypoxic conditions.
Once normal oxygen tension is restored, HIF is
quickly degraded in a process mediated by pVHL.
For the pVHL protein to interact with HIF and
mediate its degradation, it must first bind other sig-
naling intermediaries known as elongin b and c and
Cul2 [18]. These molecules normally bind to pVHL
allowing pVHL to bind to HIF, allowing ubiquitina-
tion (ie, degradation) of HIF. The defective pVHL
protein is unable to bind to these smaller molecules or
binds only weakly. As a consequence HIF is not
degraded even in normoxic conditions. The cell acts
as if it were chronically hypoxic even under normoxic
conditions. HIF also mediates the production of a
number of downstream growth factors. These include
vascular endothelial growth factor, which is one of the
P.L. Choyke / Radiol Clin N Am 41 (2003) 10371051 1039
critical growth factors in early tumor angiogenesis.
Vascular endothelial growth factor has been a target
molecule for the first generation of antiangiogenic
treatments. One of the mechanisms of tumor devel-
opment in VHL may be the failure of pVHL to
suppress HIF leading to unregulated production of
vascular endothelial growth factor and angiogenesis.
[14,19]. Unregulated vascular endothelial growth fac-
tor may account for the highly vascular nature of clear
cell tumors of the kidney. HIF also stimulates the
production of erythropoietin, glucose transporters
(GLUT1), and nitric oxygen synthase. This could also
explain why some tumors in VHL produce excess
erythropoietin. Interestingly, when antibodies to vas-
cular endothelial growth factor were administered to
patients with VHL in a clinical trial, erythrocytosis
secondary to erythropoietin overproduction was
observed [20,21]. By blocking one pathway (vascular
endothelial growth factor), another (erythropoietin)
was overexpressed.
Avariety of mutations of the VHL gene have been
discovered including complete and partial deletions,
single missense mutations, and frame shift mutations.
Fortunately, patients suspected of the disease can now
be tested for VHL with a simple blood sample. DNA
from peripheral white cells is used to check for
recorded mutations in VHL. The test is 99% accurate
for the diagnosis of VHL [22].
Renal lesions are a common manifestation of
VHL. Between 60% and 70% of patients develop
cysts in the kidney and about 40% develop radio-
logically evident renal cancers (Fig. 2). If one exam-
ines the normal-appearing tissue of a kidney from a
patient with VHL one finds hundreds of small tumor-
lets scattered throughout the parenchyma, invisible to
the naked eye (Fig. 3) [23]. That only a few of many
tumors grow to visible tumors on CT is one of the
unusual features of VHL. Tumors can take many
forms in VHL. They can appear as cysts, cystic renal
cancers, and solid renal cancers [24]. The cell lining
of even a simple renal cyst in VHL contains clear
cells similar in appearance to those found within clear
cell carcinomas.
Cysts can regress or grow. The solid components
of mixed lesions tend to grow over time, whereas the
cystic areas remain unchanged or regress. Solid
lesions tend to grow progressively [25]. Occasionally,
heavily calcified or hemorrhagic cystic disease is
seen. Both are usually associated with less aggressive
forms of renal cancer but this is not universally true.
Fig. 1. The cell types of renal cancer. (A) Clear cell carcinoma. (B) Type I papillary renal cancer. (C) Type II papillary renal
cancer. (D) Chromophobe carcinoma. (E) Oncocytoma.
P.L. Choyke / Radiol Clin N Am 41 (2003) 10371051 1040
Renal cancers in VHL tend to be well differen-
tiated or Furman grade I to II when they are under
3 cm in diameter. Only one report of a metastatic
renal tumor less than 3 cm in diameter (2.5 cm) has
appeared in the literature [26]. As a consequence, it is
generally believed that treatment should be reserved
for patients with larger lesions, greater than or equal
to 3 cm in diameter. This strategy has been very
successful in preserving renal function while avoid-
ing metastatic disease [27,28].
Renal cancers are typically detected and measured
on serial contrast-enhanced CT scans (see Fig. 2).
Using multidetector CT, unenhanced images through
the liver and kidneys are first obtained with 5-mm
collimation. A bolus of intravenous iodinated contrast
(130 mL of a nonionic contrast agent) can be adminis-
tered at 3 mL/second and 2.5-mm thick sections
(reconstructed at 5-mm intervals) are obtained during
the arterial phase (approximately 25 seconds) and
during the venous phase (approximately 80 seconds).
The precontrast scans are useful for judging whether
a lesion is actually enhancing and are of particular use
when a hemorrhagic cyst is present. Arterial phase
images are useful for detecting pancreatic neuro-
endocrine tumors (found in approximately 10% to
15% of VHL patients), which enhance intensely only
on the arterial phase, whereas the venous phase is the
most important phase for evaluating the kidneys. The
adrenals are equally well seen on all three phases.
Three-dimensional CT angiography and reconstruc-
tion can also be performed as clinically necessary
before surgery where a three-dimensional model of
the kidney can be made to assist the surgeon in
identifying lesions for removal.
Serial CT imaging is recommended for patients
with VHL even if they have minimal or no renal
disease. The lifetime risk of renal cancer is high in
VHL and the key to preserving renal function and
preventing metastatic disease is careful monitoring of
Fig. 3. Clear cell tumorlet in the parenchyma of a patient
with von Hippel-Lindau disease. Note that there is a tiny
focus of tumor within the renal parenchyma (arrow).
Hundreds of these lesions are found in the kidneys of
patients with VHL.
Fig. 2. (A, B) Von Hippel-Lindau disease. This 32-year-old
man has bilateral solid and cystic renal masses. The solid
lesions proved to be clear cell carcinomas.
P.L. Choyke / Radiol Clin N Am 41 (2003) 10371051 1041
the patient [29]. Patients with minimal disease can be
scanned at 1- to 2-year intervals, whereas patients
with active renal tumors need to be seen more fre-
quently (every 6 to 12 months). In patients with
lesions of borderline size (approximately 3 cm) even
more frequent studies may be performed. Tumor
growth is not always linear and predictable and for
this reason the record of past CTs is not necessarily
predictive of the future for any given lesion. CT is the
preferred method of screening because it is relatively
less expensive than MR imaging and the appearance
of renal masses is well understood. MR imaging with
gadolinium chelate enhancement is a viable alterna-
tive in patients with poor renal function, those wishing
to avoid ionizing radiation, or severe allergy to iodin-
ated contrast media. This should be performed with a
torso array coil and fat suppression. Attempts should
be made to measure the lesion before and after
contrast using the same parameters [30]. Ultrasound
is less accurate than other techniques for detecting and
characterizing renal masses in VHL and should not be
relied on exclusively [31].
Why wait to treat known tumors within the
kidney in a patient with VHL? This is a conscious
strategy based on the knowledge that VHL is a
lifelong disorder that must be managed differently
than sporadic disease [28]. Preservation of renal
function must be balanced against the risk of meta-
static renal cancer. Partial nephrectomy is the method
with the longest track record. Unfortunately, with
every partial nephrectomy there is inevitably some
loss of renal function and scarring, which makes
subsequent surgeries even more difficult. As a con-
sequence, surgeries should be spaced as far apart
from each other as possible in the hopes of pre-
serving renal function for the longest possible inter-
val. It is recommended that partial nephrectomies not
be performed until the solid component of the largest
tumor is 3 cm or more.
The standard method of treatment of renal tumors
in VHL is nephron-sparing surgery [27]. In this
procedure, the surgeon enucleates visible tumors
and cysts on the renal surface. Deeper lesions are
detected using intraoperative ultrasound (Fig. 4) [32].
The purpose of the nephron-sparing approach is
to remove the relevant lesions while maximally pre-
serving renal parenchyma. Of course, there is a limit
to the number of procedures that can be performed on
a single kidney and completion nephrectomies are
sometimes necessary. If the patient is discovered too
late for nephron-sparing approaches, a total nephrec-
tomy may be necessary.
Recently, radiofrequency ablation and cryotherapy
have been used because they are comparatively
minimally invasive methods for treating small renal
cancers in VHL and other hereditary renal masses
[3335]. For lesions positioned close to the bowel,
laparoscopically guided radiofrequency ablation or
cryotherapy can be performed (Fig. 5) [3638].
Although no studies documenting improved survival
or enhanced renal function have been reported, it
seems reasonable that these approaches result in less
damage to the kidney. Because the tumor is not
treated under direct vision, however, it also is
possible that the tumor may be incompletely treated.
For this reason close follow-up with imaging studies
of treated lesions is important after radiofrequency
ablation or cryotherapy [37,38]. It is important to
realize that an untreated remnant of tumor measur-
ing 5 mm in diameter from a tumor that was
originally 3 cm behaves biologically like a 3-cm
lesion and not a 5-mm tumor. As a consequence,
early retreatment of recurrences is recommended.
Although radiofrequency ablation and cryotherapy
are attractive alternatives, long-term experience is
still lacking.
Hereditary papillary renal carcinoma
Hereditary papillary renal cancer (HPRC) is an
autosomal-dominant hereditary condition in which
the kidneys develop multiple, bilateral type I papil-
lary renal cancers. No other extrarenal manifestations
have been reported in this syndrome. Sporadic type I
papillary renal tumors have a better prognosis than
other cell types, so it is not surprising that the tumors
associated with HPRC tend to be slow growing and
rarely cause death [39]. Because of the favorable
prognosis of HPRC, the patient may not come to
medical attention and the disease often is not diag-
nosed until the patient is in their fifth decade. In
VHL, the patient is often diagnosed in their teens
and twenties.
The gene responsible for HPRC has been located
at 7q 31.3 and is known as the c-MET proto-onco-
gene [40]. This gene was first described in 1984 but
was only recently linked to renal cancer [41]. Unlike
VHL where it is thought that a mutation leads to
lower levels of the VHL protein, c-MET seems to be
overexpressed in type 1 papillary tumors. The gene
codes for a transmembrane tyrosine kinase, which
acts as a receptor for hepatocyte growth factor. The
mutations associated with HPRC are found on the
extracellular portion of the transmembrane protein
where hepatocyte growth factor interacts with the
receptor. The mechanism by which the mutated
protein causes tumor formation, however, is still
P.L. Choyke / Radiol Clin N Am 41 (2003) 10371051 1042
unknown. Interestingly, alterations in the hepatocyte
growth factor receptor have also been found in VHL-
related tumors [42]. Moreover, there is some evidence
that sporadic papillary renal tumors found in the
general population that have c-MET alterations are
more biologically aggressive [42]
Unlike clear cell carcinomas of VHL that are
highly vascular on contrast-enhanced CT, the lesions
of HPRC tend to be hypovascular (Fig. 6). Indeed, if
density measurements are not obtained carefully,
some lesions may be mistaken for cysts [41,43].
The change in enhancement before and after intra-
venous contrast media can be as little as 10 to 15 HU.
This places a premium on obtaining scans of high
quality with the same technique (kilovolt [peak],
milliamp, slice thickness, field of view, and so forth)
both before and after contrast media administration.
The CT protocol used in these cases is the same one
used for VHL patients, namely precontrast, arterial,
and venous phase postcontrast helical CT. Enhance-
ment on MR imaging after gadolinium chelate ad-
ministration is often very modest (15% to 20% over
baseline) [30,43]. Renal sonography can be mislead-
ing because the lesions are often isoechoic when they
are less than 3 cm in diameter and sonography should
not be used to monitor patients with HPRC [43].
Hereditary papillary renal cancer can be suspected
in a patient with two or more poorly enhancing renal
masses. Renal cystic disease is not usually a feature of
the disease but incidental cysts can occur in HPRC. If
the patient has a family history of renal cancer and
particularly if the cell type is papillary type I, the
presumptive diagnosis of HPRCcan be made. This can
be confirmed with genetic testing of peripheral blood.
Fig. 4. Intraoperative ultrasound of a mixed solid and cystic
lesion within the kidney. Note that the mass is below the
surface of the kidney (arrows) and is not visible to the
surgeon. Intraoperative ultrasound assists the surgeon by
demonstrating the parenchyma deep to the surface.
Fig. 5. Patient with von Hippel-Lindau disease successfully
treated with laparoscopically assisted radiofrequency abla-
tion. Note a solid lesion (arrow) on the pretreatment study
(A) has become nonenhancing and smaller 6 months after
treatment with RF ablation (B). Cystic disease is also present
in the head of the pancreas.
P.L. Choyke / Radiol Clin N Am 41 (2003) 10371051 1043
Treatment of HPRC renal tumors is similar to
VHL. It is generally believed that surgery can be
delayed until one of the tumors reaches 3 cm in
diameter and that renal-preserving surgery should be
attempted whenever feasible. If the tumor is found at
a diameter greater than 3 cm every attempt should be
made to perform a nephron-sparing procedure. If that
is not possible, however, a nephrectomy may be
required. Alternatively, minimally invasive radiofre-
quency ablation or cryoablation may be suitable in
some patients. In general, the prognosis for HPRC is
considered excellent and many patients live normal
lives with this condition. The radiologist, however,
should be alert to the possibility of HPRC when
multiple or bilateral low-density solid renal tumors
are seen.
Hereditary leiomyoma renal cell carcinoma
Hereditary leiomyoma renal cell carcinoma
(HLRCC) is an autosomal-dominant genodermatosis
that causes cutaneous leiomyomas, uterine leiomyo-
mas, and type II papillary renal cancers. The syn-
drome, originally described in Finland among families
with hereditary uterine leiomyoma, has now been
seen throughout Europe and North America. The
association of cutaneous and uterine leiomyomas is
known as Reeds syndrome but the association with
renal tumors is only recent [44]. The hallmarks of
HLRCC are (1) cutaneous leiomyomas over the trunk
and extremities and more rarely the face; (2) uterine
fibroids at an early age (< 30 years); and (3) type II
papillary renal tumors.
The gene for HLRCC is found on the first
chromosome (1q42.3) and is known as fumarate
hydratase. Interesting, this enzyme is a critical step
in the Krebs tricarboxylic acid cycle but its role in
causing renal tumors is not understood. Fumarate
hydratase likely acts as a tumor suppressor because
fumarate hydratase enzyme activity is low or absent
in tumors found in HLRCC [45].
Type II papillary renal cancers are found in about
17% of individuals with HLRCC and can be clini-
cally aggressive (Fig. 7). Metastases are seen in over
half of cases even with relatively small primary
tumors. HLRCC renal tumors differ from the other
hereditary renal cancer syndromes in several impor-
tant ways. Histologically, they appear to be type II
papillary tumors except for the occasional collecting
duct renal cancer. The renal tumors in HLRCC are
usually solitary and unilateral as opposed to the other
syndromes, where the tumors are usually multiple
and bilateral. The tumors are also substantially more
aggressive with Furman nuclear grades of 3 or 4 in all
cases reported and a tendency to metastasize even
when small (see Fig. 7). In contrast, the tumors
associated with VHL and HPRC are typically only
Furman nuclear grade 1 or 2 and these tumors rarely
metastasize when less than 3 cm in diameter. It is
particularly important to differentiate HLRCC from
HPRC. Whereas one might follow a patient with
HPRC with watchful waiting, treatment is more
Fig. 6. (A) Precontrast CT; (B) postcontrast CT. Patient with
hereditary papillary renal cancer demonstrates a poorly
enhancing mass in the right kidney. This lesion increased in
CT attenuation by only 12 HU after intravenous contrast.
Minimally enhancing solid tumors are typical of the tumors
found in HPRC.
P.L. Choyke / Radiol Clin N Am 41 (2003) 10371051 1044
urgent in patients with HLRCC. Tumors should be
removed when they are first seen.
Uterine fibroids occur in over 90% of women with
HLRCC. Most of these women also had skin leio-
myomas. Almost half the women with HLRCC
require a hysterectomy by the age of 30 (see Fig. 7).
In addition to screening for renal cancers patients
should be screened for uterine leiomyomas and
leiomyosarcomas. It is thought that this entity has a
higher frequency of transformation to malignant
leiomyosarcoma within the uterus, although criteria
for distinguishing these transformations by imaging
are lacking [45]. Although the cutaneous leiomyomas
do not degenerate into malignancies in general, a few
cases of cutaneous leiomyosarcomas have been
reported [45]. The cutaneous manifestations become
more prominent with age; they are hardly noticeable
when the patients are young but can become a cos-
metic issue when the patient reaches 30 to 40 years
of age.
CT is used to screen for HLRCC renal cancers and
assess the status of the uterus. Interestingly, although
the tumors tend to be hypovascular like type 1
papillary tumor, they are much more lethal. Careful
screening for metastatic disease should be performed.
MR imaging and ultrasound are suitable substitutes
when contrast-enhanced CT cannot be performed.
MR imaging of the uterus is particularly helpful in
detecting and characterizing uterine leiomyomas.
Birt-Hogg-Dube syndrome
Birt-Hogg-Dube syndrome (BHD), an autosomal-
dominant disorder, was originally described as a
dermatologic disorder characterized by fibrofollicu-
lomas (growths in the hair follicles) of the face and
trunk [46]. Later it became clear that there were other
markers for the disease including pulmonary cysts
and renal tumors [47,48]. The pulmonary cysts vary
in severity and size from one or two small, scattered
cysts to severe cystic disease complicated by sponta-
neous pneumothoraces, which may be refractory to
conventional pleurodesis. Between 15% and 30% of
patients with BHD develop renal cancers. The renal
tumors seen in BHD are commonly, but not always,
chromophobe carcinomas or oncocytomas. Both clear
cell and papillary tumors have also been seen in BHD
[34]. Approximately 34% of the tumors are charac-
terized as chromophobe carcinomas and about 50%
are hybrid chromophobe-oncocytomas. The remain-
der are oncocytomas (5%); clear cell carcinoma (9%);
and papillary renal cancer (2%) [34]. A higher rate of
colonic polyps have been observed in some families
but the risk for colon cancer has not been clearly
defined [49,50].
The gene for BHD is located at 17p11.2 and codes
for a protein named folliculin [48,49]. Little is known
of the mechanism of tumor formation or the function
of folliculin. It is thought that this gene acts as a
tumor suppressor and acts as a structural protein in
Fig. 7. Hereditary leiomyoma renal cell carcinoma. (A) A
small mass (3 cm) is present in the middle portion of the left
kidney. It is poorly enhancing typical of papillary renal
cancer; however, in addition there is a metastatic lympha-
denopathy (arrow) adjacent to the aorta. This proved to be a
papillary type II renal cancer. The renal lesion was not
visible on ultrasound. (B) Abdominal CT in another patient
(aged 32) with HLRCC demonstrates multiple enhancing
leiomyomas within the uterus.
P.L. Choyke / Radiol Clin N Am 41 (2003) 10371051 1045
the lung where it may form a component of the
cytoskeletal network. This might explain the tend-
ency of BHD patients to develop lungs cysts. The
Hornstein-Knickenberg syndrome overlaps BHD and
is now considered to be part of BHD [51]. BHD
differs from other forms of hereditary renal cancer in
that it produces a variety of cell types of renal cancer,
not just one but chromophobe cancers and their
variants predominate. The chromophobe tumors and
oncocytomas also arise from the distal renal tubules
in contrast to VHL and HPRC-related tumors that
arise from the proximal tubules [48].
The imaging of BHD should always include scans
of the lungs and abdomen (Fig. 8). The pulmonary
cysts are generally found in the lower lobes and vary
in size and number from a few to multiple. Pneumo-
thoraces may be seen despite the absence of symp-
toms. Although severe cystic disease is present in
some individuals the patients do not usually become
oxygen-dependent. This differs from the cystic lung
disease found in lymphangioleiomyomatosis asso-
ciated with tuberous sclerosis (TS, see later). The
chromophobe or mixed cell types typically demon-
strate moderate uniform enhancement on CT, which
is different in appearance from VHL-associated
tumors, which typically have cystic components.
Birt-Hogg-Dube syndrome is managed in a man-
ner similar to VHL. Tumors are generally observed
until they reach 2 to 3 cm diameter, whereupon
nephron-sparing surgery is performed. Chromophobe
carcinomas tend to be highly enhancing and are
relatively homogeneous in appearance. Radiofre-
quency ablation or cryotherapy also can be consid-
ered, although little outcome data are yet available.
Familial renal oncocytoma
Familial renal oncocytoma (FRO) is an incom-
pletely characterized condition in which affected
individuals develop renal oncocytomas [8]. The term
familial is used instead of hereditary to denote
that a clear hereditary pattern has not yet been
established. Five families with a hereditary predispo-
sition to renal oncocytomas were first described
by Weirich et al in 1998 [52]. Some families had
Fig. 8. Birt-Hogg-Dube syndrome. (A) Contrast-enhanced CT demonstrates an enhancing mass in the right kidney typical of a
chromophobe carcinoma. (B) Additional smaller lesion is present in the lower pole. (C) Pulmonary CT demonstrates multiple
cysts and a loculated pneumothorax (arrow). This patient had experienced multiple pneumothoraces as a consequence of cystic
lung disease.
P.L. Choyke / Radiol Clin N Am 41 (2003) 10371051 1046
extensive bilateral disease, and compromised renal
function [11]. Other families had mild manifestations
of FRO. There may be some overlap with BHD
because several families initially considered to have
FRO proved to have features of BHD. Renal dys-
function without extensive neoplastic disease was
also noted in some family members. The prevalence
of this entity is unknown and no putative genetic
locus has yet been identified.
The diagnosis is based on the identification of
multiple oncocytomas in one or more family mem-
bers. By imaging, the lesions are indistinguishable
from malignant renal cancers and must be treated as if
they were renal cancers (Fig. 9) [53]. When onco-
cytomas are extensive and confluent the term renal
oncocytosis can be applied [11]. Because renal
function is often compromised these patients are
often scanned with MR imaging using gadolinium-
based contrast agents. Lifelong monitoring with
imaging studies is recommended, although compli-
ance is lower because the perceived risk by the
patient is reduced.
Medullary carcinoma
Medullary carcinoma of the kidney is a rare
aggressive neoplasm that develops in young, black
patients (age range, 11 to 39 years) with sickle cell
trait [54]. This has led some observers to comment
that the renal tumors may be a secondary complica-
tion of sickle cell trait [55]. This seems doubtful
because the sickle cell trait produces only mild
symptoms and the youth of the patients (median
age about 20 years) makes it unlikely to be the result
of a chronic process. The rate of renal tumor develop-
ment even among people with sickle cell trait is low.
Approximately 1 in 12 blacks have Hb AS (sickle cell
trait) and relatively few reports of medullary carci-
noma of the kidney have been published [56]. The
risk of developing medullary carcinoma of the kidney
even in the presence of sickle cell trait is negligible.
The sickle cell gene is located at 11p15.
Unfortunately, the tumors at presentation tend to
be large and are often metastatic. The tumor is
generally advanced by the time it is discovered;
median survival from the time of diagnosis is only
15 weeks [57]. Surgery seems to be useful only in
providing palliation.
The tumors are generally large, central, and hetero-
geneous in character. There is often evidence of ade-
nopathy or pulmonary metastases. These tumors
should be evaluated with MR imaging or CT before
surgery to provide accurate clinical staging (nodal
and inferior vena caval involvement). Systemic thera-
pies are recommended but have failed significantly to
modify the course of the illness.
Other syndromes
Tuberous sclerosis
Tuberous sclerosis is a genetic disease character-
ized by hamartomas in the skin, brain, and viscera.
Although not technically considered a cancer syn-
drome, TS is associated with an increased risk of
renal malignancy. TS has prevalence in the popula-
tion of approximately 1:10,000. The most common
manifestations of TS in the kidneys are cysts and
angiomyolipomas. Approximately a third of angio-
myolipomas may not contain fat visible by CT and
are difficult to differentiate from cancer. Most often
the mass represents a nonfatty angiomyolipoma.
Approximately 1% to 2% of patients with TS develop
renal cancers, which is substantially higher than the
expected rate of renal cancer in the general popula-
tion [58,59].
There is a complex relationship between renal
cancer and TS. Renal cancers are found with in-
creased frequency in patients with TS compared with
the general population and have been identified with
mutations in both TSC1 and TSC2, the two gene loci
associated with TS [59,60]. Occasionally, renal can-
cers are even the presenting sign of TS [61]. Multi-
focal renal cancer has been found in siblings from a
Fig. 9. Hereditary renal oncocytoma. Bilateral renal oncocy-
tomas are present in this patient. Note that the lesions are
homogeneously enhancing. Stellate central scars, seen com-
monly in sporadic oncocytomas, are unusual in this condition.
P.L. Choyke / Radiol Clin N Am 41 (2003) 10371051 1047
single family with TSC1 [62]. Features indicating an
association with renal cancer include a striking
female predominance (81% female versus 70% male
predominance for sporadic renal cancers); median
age of only 28 years (versus sixth and seventh
decades for sporadic renal cancers); multifocality;
and bilaterality (43%) [63,64]. Supportive evidence
comes from the animal model of TS, the Eker rat,
which has an insertional mutation in the rat TSC2
gene. The Eker rat develops tumors (adenomas and
carcinomas) and cysts in the kidney [65]. Avariety of
cell types of renal cancers have been reported in
humans with TS including clear cell (most common)
papillary and chromophobe carcinomas [66,67].
Oncocytomas have also been reported with increased
frequency in TS [68]. Some doubt has been raised
concerning the actual origin of some renal tumors in
TS because some lesions may actually be malignant
epithelioid angiomyolipomas, which can mimic renal
cancers [69].
Translocation of chromosome 3
A number of families have been reported in which
part of the short arm of chromosome 3 has been
translocated to another chromosome [9,17]. These
balanced translocations predispose the patient to the
development of clear cell carcinomas of the kidney.
Because VHL is also located on chromosome 3 it was
originally assumed that this was a subset of VHL;
however, patients with chromosome 3 translocation
do not have other stigmata of VHL and the VHL
portion of the short arm of chromosome 3 is often
intact [70,71]. Translocation of the chromosome 3
can result in a clear-cell predominant form of heredi-
tary renal cancer. Unlike the other syndromes, which
require a careful analysis of the genes for mutations,
this abnormality can be detected on a karyotype of
peripheral white blood cells.
Familial renal cancer
Not all families with tendencies to develop renal
cancers are explained by the syndromes described
previously. As a result, the term familial renal
cancer is used to characterize patients with apparent
genetic predisposition to renal cancer in whom the
exact gene involved has not yet been determined.
Fortunately, as more is learned about the origins of
hereditary renal cancer this category contains fewer
patients and more are successfully characterized by
specific diagnoses.
Summary
Over the past 5 years there have been dramatic
developments in the extent of knowledge of heredi-
tary renal cancers. In addition to VHL, which is
associated with clear cell carcinoma, one can now
list HPRC (associated with type I papillary renal
cancer) and HLRCC (associated with type II papillary
renal cancer). BHD and FRO are associated with
chromophobe carcinoma and oncocytomas, although
other histologic tumor types have been found in
BHD. Medullary carcinoma of the kidney is asso-
ciated with sickle cell trait. Although the genes
associated with these tumors have been discovered,
the exact mechanisms by which they cause renal
cancer remain to be elucidated. It is quite likely that
other genes also are involved in this process. Using
VHL as an example, research is now underway on
targeting mutant pVHL or excess HIF for diagnostic
and therapeutic purposes. Understanding the mecha-
nisms leading to cancer may open new targets of
opportunity for drug development. This improved
knowledge of the biogenetic pathways used to form
tumors will impact the development of new thera-
peutic techniques for treating renal cancers in heredi-
tary and nonhereditary forms of the disease.
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P.L. Choyke / Radiol Clin N Am 41 (2003) 10371051 1051
Surgical management of renal tumors
Rizk El-Galley, MB Bch, FRCS
Department of Surgery, Division of Urology, University of Alabama at Birmingham, 1530 3rd Avenue South, MEB 602,
Birmingham, AL 352943296, USA
Renal cell carcinoma is a relatively rare tumor,
accounting for approximately 3% of malignancies in
adults, but is the most common tumor of the kidney
and the third most common tumor seen by urologists
[1]. The classic symptom triad of pain, hematuria,
and flank pain is certainly a reliable clinical symptom
complex. More recently, however, most renal cell
carcinomas are diagnosed at earlier stages and are
frequently found incidentally at radiologic investiga-
tion done for other reasons [2].
Renal cell carcinoma is refractory to most tradi-
tional oncologic treatments, including chemotherapy,
radiation therapy, and hormonal therapy [35]. Radi-
cal nephrectomy, removing all the contents of Ge-
rotas fascia, is considered the standard treatment for
localized tumors. More recent data indicate, however,
that in carefully selected patients partial nephrectomy
may be an option [68]. The role of radical nephrec-
tomy in patients with metastatic disease is contro-
versial and is not indicated unless the patient has
intractable bleeding or pain, or it is necessary to debulk
the tumor for immunotherapy or other systemic thera-
pies. Local extension into the renal vein or inferior
vena cava (IVC) is not considered a contraindication to
radical nephrectomy. Tumor extension beyond Gero-
tas fascia involving other organs is associated with
poor prognosis, however, and nephrectomy should be
considered only for palliation or as part of an adjuvant
therapy protocol [912].
Because of recent advances in sophisticated ra-
diologic studies, the surgeon can now make an
accurate preoperative assessment of the nature and
extent of kidney tumors. The diagnosis of renal cell
carcinoma is generally made with CT, showing a
solid mass in the parenchyma of the kidney. Fewer
than 5% of all renal cell carcinomas have a cystic
appearance with septations, irregular borders, dystro-
phic calcification, or other features that distinguish it
from a simple renal cyst.
The differential diagnosis of solid kidney masses
includes oncocytoma (granular oncocytes on histo-
logic analysis, with a central scar in the tumor);
angiomyolipoma (contains fat, seen on CT scans);
xanthogranulomatous pyelonephritis (usually in pa-
tients with diabetes, with a concurrent stone in a
poorly functioning kidney); fibromas; or metastasis.
Despite the diagnostic clues seen at radiologic inves-
tigation, the histologic nature of these masses cannot
be confirmed without tissue biopsy, which is gener-
ally avoided because of the risk for seeding malignant
cells through the needle track or the possibility of
obtaining benign tissue approximating a malignant
area. Accordingly, in most of these patients radical
nephrectomy is required before the kidney lesion is
finally diagnosed pathologically.
CT and MR imaging are the imaging studies most
commonly used to stage renal tumors. Abdominal CT
is particularly useful to show local extension of tumor
and the presence of enlarged para-aortic lymph nodes.
MR imaging is superior to CT for determining the
superior extent of a vena caval thrombus; however,
the new generation of CT scanners with rapid image
acquisition are as accurate as MR imaging in vena
caval imaging [13,14]. These new imaging studies
have replaced, to large extent, venocavography and
arteriography, which are more invasive. Chest radiog-
raphy or chest CT is routinely done to rule out
pulmonary metastasis; bone scanning is required only
in the presence of a large tumor or if clinical evalua-
tion suggests metastasis to bone.
When evaluating renal tumors, the urologist is
looking for certain information to help in constructing
0033-8389/03/$ see front matter D 2003 Elsevier Inc. All rights reserved.
doi:10.1016/S0033-8389(03)00077-0
E-mail address: rizk.el-galley@ccc.uab.edu
Radiol Clin N Am 41 (2003) 10531065
a management plan. Here are some of the points that
contribute in the surgical decision-making.
Is it a kidney a tumor or a pseudotumor?
Pseudotumors in the kidney are rare; however, this
diagnosis should be taken into consideration. A
hypertrophied column of Bertin, inflammatory renal
mass, or perinephric inflammation extending to the
kidney may be confused with a renal tumor. A CT
scan is usually very helpful in delineating the nature
of these tumors. In some cases, when the nature of the
mass in undetermined, a repeat CT a few weeks later
shows a significant change in an inflammatory mass,
whereas a tumor change is less remarkable. A hyper-
trophied column of Bertin has been a diagnostic
problem on intravenous pyelogram and a dimercap-
tosuccinic acid (DMSA) nuclear scan was required to
establish the diagnosis; a column of Bertin is homog-
enous with the rest of the kidney tissue, whereas a
tumor shows different isotope uptake. Most of these
swellings, however, can be differentiated with a CT
scan that obviates the need for a nuclear scan [15,16].
Is it a cystic tumor?
Cystic renal masses range from a simple cyst to
cystic renal carcinoma. Characterization of cystic
renal masses relies mainly on the Bosniak classifica-
tion, which consists of four categories [1719]:
benign simple cysts (category I); minimally compli-
cated cysts (category II); indeterminate cystic renal
masses that include cystic renal tumors (multilocu-
lated or not) and complex cysts (category III); and
cystic renal cell carcinomas (category IV). Usually,
category I cysts are not indication for surgery unless
they are symptomatic, category II are most likely
benign and can be watched, category III are more
likely to be malignant, and category IV are highly
suspicious for being malignant [20,21].
Is it a solid renal tumor?
In general, solid renal tumors should be consid-
ered malignant until proved otherwise, with the
exception of a tumor that contains fat on the CT
scanning (angiomyolipoma) or tumors that do not
enhance on a CT and do not grow on follow-up CTs.
Oncocytoma is another tumor that is difficult to
differentiate from malignant tumors radiologically
and is usually diagnosed after excision [22].
Surgical planning is usually dependent on radio-
logic information. The extent of the tumor and its
location in the kidney, proximity to the renal collecting
system and renal vessels, and presence of fat planes
between the tumor and other structures (eg, liver,
colon, and posterior abdominal wall muscles) are all
important information that help the surgeon to assess
the local invasiveness of the tumor. Similarly, tumor
extension into the renal vein or IVC and the level of
this extension are essential information in surgical
decision-making. Tumors that extend beyond the distal
two thirds of the renal vein are not suitable for
laparoscopic surgery. The level of extension in the
IVC should be assessed accurately before surgery.
Tumors that extend above the hepatic veins require
full mobilization of the liver to control the IVC above
the hepatic veins. It also requires the Pringle maneuver
(clamping the porta hepatis), clamping the renal veins
and the lumbar veins to reduce blood loss during tumor
extraction from the IVC. Tumors that extend into the
right atrium require the involvement of a cardiotho-
racic surgeon and cardiopulmonary bypass to extract
the tumor from the IVC and atrium. The presence of
intra-abdominal metastasis, the function of the contra-
lateral kidney, and the appearance of the adrenal glands
are valuable information for surgical decision making.
Surgical anatomy of the kidneys
The kidneys are paired, reddish brown, solid
organs situated on each side of the midline in the
retroperitoneal space. Their weight depends on body
size, averaging 150 and 135 g each in the adult man
and woman, respectively. Kidneys in mature adults
vary in length from 11 to 14 cm, in width from 5 to
7 cm, and in thickness from 2.5 to 3 cm. Because of
the effect of the hepatic mass, the right kidney is
shorter and broader and lays 1 to 2 cm lower than the
left kidney.
Each kidney is surrounded by a layer of fat, covered
by the Gerotas fascia (Fig. 1). Gerotas fascia is
completely fused above and lateral to the kidney;
medially and inferiorly fusion is incomplete. This
incomplete fusion is of clinical importance in deter-
mining the possible routes of spread of bleeding or
infection around the kidneys. Both layers of Gerotas
fascia probably continue across the midline, with the
posterior layer crossing behind the great vessels and
the anterior layer extending in front of the great
vessels. The parietal peritoneumfuses with the anterior
layer of Gerotas fascia to form the white line of Toldt
laterally. During surgical approaches to the kidneys,
incision along this line enables the surgeon to reflect
R. El-Galley / Radiol Clin N Am 41 (2003) 10531065 1054
the peritoneum with the mesocolon through a relative-
ly bloodless plane and gives access to the renal hilum.
The upper pole of the left kidney lies at the level
of the twelfth thoracic vertebral body and the lower
pole at the level of the third lumbar vertebra (Fig. 2).
The right kidney usually extends from the top of the
first lumbar vertebra to the bottom of the third lumbar
vertebra. Because of the free mobility of the kidneys,
these relationships change with both body position
and respiration.
The right adrenal gland covers the uppermost part
of the anteromedial surface of the right kidney. The
anterior relationships of the right kidney include
the liver, which overlies the upper two thirds of the
anterior surface, and the hepatic flexure of the colon,
which overlies the lower third. The right renal hilum
is overlaid by the second part of the duodenum. The
anterior surface of the kidney beneath the liver is the
only area covered by peritoneum. The anteromedial
surface of the left kidney is also covered by the left
adrenal gland in its uppermost part. The spleen, body
of the pancreas, stomach, and splenic flexure of the
colon are all anterior to the left kidney. The area of
the kidney beneath the small intestine, the spleen, and
the stomach is covered by peritoneum. Both kidneys
share relatively symmetric relations to the posterior
abdominal wall. The upper third or upper pole of each
kidney lies on the diaphragm, behind which is the
pleural reflection. An operative approach to this area
with a high incision above the eleventh or tenth rib
risks entering the pleural space. The upper border of
the left kidney usually extends to the upper border of
the eleventh rib, and the upper pole of the right
kidney, which is lower, is usually at the level of the
eleventh intercostal space. The lower two thirds of the
posterior surface of both kidneys lies on three
muscles, which from medial to lateral are the psoas
major, quadratus lumborum, and the aponeurosis of
the transversus abdominis muscles. The renal vessels
and pelvis lie against the contour of the psoas muscle,
which tilts the lower pole of each kidney away from
the midline. Alterations in this alignment may be seen
with space-occupying lesions and should prompt
careful assessment.
The renal parenchyma is divided into an internal
darker medulla and an external lighter-hued cortex
(Fig. 3). The medulla is composed of 8 to 18 conical
structures called the renal pyramids, which are
made of ascending and descending loops of Henle
and collecting ducts. The round tip of each pyramid is
known as the renal papilla. These papillae cannot be
seen during surgical dissections because each papillary
projection is encompassed by a smooth muscular
sleeve called a minor calyx. These minor calyces
Fig. 1. Gerotas fascia. (From El-Galley RES, Keane TE. Kidneys, ureters, and bladders. In: Wood WC, Skandalakis JE, editors.
Anatomic basis of tumor surgery. St. Louis: Quality Medical Publishing; 1999; with permission.)
R. El-Galley / Radiol Clin N Am 41 (2003) 10531065 1055
coalesce to form two or three major calyces, which in
turn join to form the renal pelvis. The renal pelvis
extends through the renal hilum behind the renal
vessels and continues as the ureter. Anatomic varia-
tions in the renal pelvis are not uncommon. The renal
pelvis, which is usually partially extrarenal, may lie
completely outside or within the kidney. Occasionally
the renal pelvis may be duplicated, with duplication of
the renal units. Anatomic variations of the renal pelvis
tend to occur bilaterally, which should be considered
when evaluating urographic studies to differentiate
pathologic conditions from normal variations.
The renal cortex lies between the bases of the
pyramids and the renal capsule. The tongues of cortical
tissue that extend between the renal pyramids are
called the columns of Bertin and, when enlarged,
can closely resemble a renal mass. The outer border of
the renal cortex should be smooth. Indentations on the
cortical surface might represent persistent fetal lobu-
lations, previous scarring, and infection or space-
occupying lesion.
Blood supply
Each kidney is classically supplied by a renal
artery and a larger renal vein, arising from the aorta
and the IVC, respectively, at the level of the second
lumbar vertebra below the takeoff of the superior
mesenteric artery (Fig. 4). These vessels enter the
renal hilum medially, with the vein anterior to the
artery and both anterior to the renal pelvis. Although
the right kidney is lower than the left kidney, the right
renal artery arises from the aorta at a higher level and
takes a longer course than the left renal artery. It
travels downward behind the IVC to reach the right
kidney, whereas the left renal artery passes slightly
upward to reach the left kidney. Because of the
posterior position of the kidneys, both renal arteries
course slightly posterior. Two small but important
branches arise from the main renal artery before its
termination in the hilum: the inferior adrenal artery and
the artery that supplies the renal pelvis and upper
ureter. Ligation of this branch may result in ischemia
Fig. 2. Location of kidneys. (From El-Galley RES, Keane TE. Kidneys, ureters, and bladders. In: Wood WC, Skandalakis JE,
editors. Anatomic basis of tumor surgery. St. Louis: Quality Medical Publishing; 1999; with permission.)
R. El-Galley / Radiol Clin N Am 41 (2003) 10531065 1056
to the area of the upper ureter with stricture formation.
The main renal artery divides into five segmental
arteries at the renal hilum. Each segmental artery is
an end artery; occlusion leads to ischemia and infarc-
tion of the corresponding renal segment. The first
branch is the posterior artery, which arises just before
the renal hilum and passes posterior to the renal pelvis
to supply a large posterior segment of the kidney. The
main renal artery then terminates into four anterior
segmental arteries at the renal hilum: (1) the apical,
(2) upper, (3) middle, and (4) lower anterior segmental
arteries (Fig. 5). Both the apical and inferior arteries
supply the anterior and posterior surfaces of the upper
and lower poles of the kidneys, respectively. The upper
and middle arteries supply two corresponding seg-
ments on the anterior surface of the kidney. Renal
vascular segments are also identified.
The segmental arteries course though the renal
sinus and branch into the lobar arteries, which are
usually distributed one for each pyramid. Each lobar
artery divides into two or three interlobar arteries that
pass between the renal pyramids to the corticomedul-
lary junction, where they become the arcuate artery.
The arcuate arteries, as their name implies, arch over
the bases of the pyramids and give rise to a series of
interlobular arteries, which in turn take a straight
course to the renal cortex, with some terminal small
branches anastomosing with the capsular arteries. This
Fig. 4. Blood supply to the kidney (anterior surface of right kidney). (From El-Galley RES, Keane TE. Kidneys, ureters, and
bladders. In: Wood WC, Skandalakis JE, editors. Anatomic basis of tumor surgery. St. Louis: Quality Medical Publishing; 1999;
with permission.)
Fig. 3. Anatomy of renal parenchyma. (From El-Galley
RES, Keane TE. Kidneys, ureters, and bladders. In: Wood
WC, Skandalakis JE, editors. Anatomic basis of tumor
surgery. St. Louis: Quality Medical Publishing; 1999;
with permission.)
R. El-Galley / Radiol Clin N Am 41 (2003) 10531065 1057
anastomosis can enlarge to supply a significant amount
of blood to the superficial cortical glomeruli, particu-
larly in cases of gradual narrowing of the renal arteries.
The renal cortex is drained by the interlobular veins,
which, unlike the renal arteries, anastomose freely with
the arcuate veins at the base of the medullary pyramids
and with the capsular and perirenal veins on the surface
of the kidney. The arcuate veins drain through the
interlobar veins to the lobar veins, which join to form
the renal vein. The right renal vein, 2 to 4 cm long,
joins the lateral aspect of the IVC, usually without
receiving any tributaries. The left renal vein, 6 to 10 cm
long, crosses anterior to the aorta and ends in the left
aspect of the IVC. It receives three tributaries lateral to
the aorta: (1) the left adrenal vein superiorly, (2) left
gonadal vein inferiorly, and (3) a lumbar vein poste-
riorly. At the renal hilum the renal vein usually lies in
front of the renal artery. Passing more medially,
however, the renal artery may be a centimeter higher
or lower than the vein.
Lymphatic drainage
Lymphatic vessels within the renal parenchyma
consist of cortical and medullary plexuses that follow
the renal vessels to the renal sinus and form several
large lymphatic trunks. The renal sinus is the site of
numerous communications between lymphatic ves-
sels from the perirenal tissues, renal pelvis, and upper
ureter. Initial, lymphatic drainage runs to the nodes
present at the renal hilum lying close to the renal
vein. These nodes form the first station for lymphatic
spread of renal cancer. On the left side, lymphatic
trunks from the renal hilum drain to the para-aortic
lymph nodes from the level of the inferior mesenteric
artery to the diaphragm. Lymphatic vessels from the
right kidney drain into the lateral paracaval and
interaortocaval nodes from the level of the common
iliac vessels to the diaphragm. Lymphatic vessels
from both sides may extend above the diaphragm to
the retrocrural nodes or directly into the thoracic duct.
Surgical applications
The kidneys can be approached through various
incisions: lumbar, anterior transperitoneal, thoraco-
abdominal, and posterior lumbar. Factors that should
be taken into consideration before selecting an inci-
sion include type of operation and pathologic condi-
tion, body habitus, and pulmonary or spinal
deformities. Small uncomplicated tumors can be
approached through an extraperitoneal flank incision.
This approach has the advantages of being extraperi-
toneal, with a shorter period of ileus, and in obese
patients most of the panniculus falls away from the
kidney. Exposure of the renal pedicle with lateral
lumbar approaches is not as good as an anterior
approach, however, and runs the risk of entering the
pleural cavity, particularly if a supracostal incision is
performed. This incision can be performed above the
twelfth or eleventh rib, either extrapleural or intra-
Fig. 5. Vascular segments (left kidney). (From El-Galley RES, Keane TE. Kidneys, ureters, and bladders. In: Wood WC,
Skandalakis JE, editors. Anatomic basis of tumor surgery. St. Louis: Quality Medical Publishing; 1999; with permission.)
R. El-Galley / Radiol Clin N Am 41 (2003) 10531065 1058
pleural, to expose the suprarenal gland or the upper
pole of the kidney, and can also be extended down-
ward to expose the ureter.
For good exposure of the renal vessels, particu-
larly for operations for advanced tumors, an ante-
rior transperitoneal approach is preferred. It can be
performed through an anterior subcostal, midline,
or paramedian incision. The midline incision is
faster to perform and to close, but the incidence
of incisional hernia is higher than with paramedian
incisions. Posterior lumbar incisions are easy to
perform and are easier on the patient, but the
exposure is limited, particularly with respect to
renal vessels. Good access is provided to the renal
pelvis and upper third of the ureter for stone
surgery, but this approach is not recommended
for malignancies.
Radical nephrectomy
The eleventh or twelfth rib supracostal incision,
with attempt to remain extrapleural, is recommended
for most cases. It provides good exposure of the
kidney, renal pedicle, and adjacent organs. Thora-
coabdominal incision is preferable in patients with
large upper pole tumors or tumors that extend into the
IVC, although median sternotomy is an option for
high caval thrombi. Unilateral anterior extraperitoneal
incision provides adequate exposure in noncompli-
cated cases. Bilateral tumors can be approached with
a midline or Chevron incision; however, such lesions
are best approached one side at a time.
On the right side, once the peritoneum is entered,
the intra-abdominal contents, mainly the liver, are
inspected for unrecognized metastasis, and the tumor
is examined carefully for resectability. The dia-
phragm is retracted superiorly with a self-retaining
retractor, and countertraction is applied to the supe-
rior border of the rib below after releasing the
costochondral ligament. The liver is kept out of the
way by gentle retraction to prevent hepatic injury.
During extensive IVC mobilization care must be
taken not to injure the short caudate veins.
Attention should be given to the renal pedicle,
which can be approached ventrally by retracting the
ascending colon and dividing the lateral paracolic
peritoneum (Fig. 6). The hepatic flexure and duode-
num are mobilized medially to expose the renal
pedicle and the renal veins lying in front of the artery.
As an alternative, with the dorsal approach to the
renal pedicle the renal artery is readily accessible for
ligation and division. This maneuver significantly
reduces potential blood loss. It can be performed by
dissecting the kidney and surrounding tissues free
Fig. 6. Approach to the renal pedicle. (From El-Galley RES, Keane TE. Kidneys, ureters, and bladders. In: Wood WC,
Skandalakis JE, editors. Anatomic basis of tumor surgery. St. Louis: Quality Medical Publishing; 1999; with permission.)
R. El-Galley / Radiol Clin N Am 41 (2003) 10531065 1059
from the posterior abdominal wall and rotating it
medially, after which the renal artery can be identi-
fied, ligated, and divided.
The ureter, gonadal vessels, and periureteral fat
are dissected free of the posterior peritoneum and
divided in two or three separate bundles. The dissec-
tion is then carried superiorly along the IVC on its
anterior surface, where there are few, if any, signifi-
cant branches.
Superior to the renal vessels the peritoneum fans
out laterally, and the dissection is performed to the
lateral border of the peritoneum. In most larger tumors
and some smaller tumors, the peritoneum cannot be
dissected free of Gerotas fascia, and the surgeon is
forced to remove a window of peritoneum with the
specimen. Care should be taken to avert injury to the
bowel, especially the C portion of the duodenum.
The superior portion of the specimen, including the
adrenal gland, should be dissected free of the retro-
peritoneum and liver. Because there may be branches
of the phrenic and other vessels at this point, the author
generally uses a series of large hemoclips, dividing the
tissue below the clips to enhance hemostasis.
On the left side, the descending colon is retracted
medially, and the lateral reflection of the peritoneum
is incised (Fig. 7). The mesentery is dissected bluntly
from the anterior surface of Gerotas fascia. Care
should be taken to prevent injury to the pancreas,
which is mobilized medially. If the tumor extends
into the colonic mesentery, this part of the mesentery
can be resected with the specimen without great risk
for colonic ischemia as long as the marginal artery is
not disrupted. The kidney and surrounding tissues are
dissected free from the posterior abdominal wall and
rotated medially, and the renal artery is identified,
ligated, and divided. In bulky tumors the superior
mesenteric artery might be displaced laterally; great
care should be taken to distinguish the superior
mesenteric artery from the renal artery on either side.
The ureter, gonadal vessels, and periureteral fat are
dissected free of the posterior peritoneum and divided
in two or three separate bundles. The dissection is then
carried superiorly along the aorta on its anterior
surface, where there are few significant branches.
The splenorenal ligament is identified, ligated, and
divided to avert splenic injury during mobilization of
the kidney. The superior portion of the specimen
should be dissected free of the retroperitoneum.
The specimen should be free at this point except for
the venous structures. The left adrenal vein drains into
Fig. 7. Kidney and surrounding tissues dissected free from the posterior abdominal wall and rotated medially. (From El-Galley
RES, Keane TE. Kidneys, ureters, and bladders. In: Wood WC, Skandalakis JE, editors. Anatomic basis of tumor surgery.
St. Louis: Quality Medical Publishing; 1999; with permission.)
R. El-Galley / Radiol Clin N Am 41 (2003) 10531065 1060
the renal vein and is ligated and divided. The back
surface of the renal vein should be inspected carefully
for any lumbar veins, which if present should be
ligated and divided. Then the renal vein should be
palpated for possible unsuspected thrombi, divided,
and ligated. Large tumors on either side frequently
develop parasitizing vessels, which are abnormal in
structure and frequently can lead to troublesome
bleeding if not ligated or clipped with great care.
Management of tumor extension in the vena cava
The presence of a solid mass in the vena cava
might represent tumor extension into the lumen,
blood thrombus, or less commonly tumor invasion
of the vena cava wall. Tumor extension into the vena
cava occurs in 4% to 10% of cases, and tumor-free
survival equivalent to survival of stage II is achieved
by complete removal of tumor extension in patients
without lymph node involvement [23]. Exploration of
the vena cava is a major procedure, and a complete
set of vascular instruments should be available. The
extent of the tumor extension into the vena cava
should be delineated preoperatively to help in plan-
ning the surgical approach. Right-sided renal tumors
with limited vena caval extension can be approached
with a right flank incision. A thoracoabdominal
incision is used for high right-sided tumor extension,
whereas a midline incision with or without a median
sternotomy extension is frequently required for
patients with left renal tumors and vena caval exten-
sion to the level of the hepatic veins or above.
Exposure of the retrohepatic vena cava is started
with division of the right triangular and coronary
ligaments of the liver and ligation of the small hepatic
(caudate) veins. The liver is then mobilized medially
to expose the vena cava, and a cardiac tourniquet is
applied around the vessel for temporary occlusion.
The contralateral renal vein and the infrarenal vena
cava also are occluded with a Rumel tourniquet.
Because about one fourth of the venous return in
the vena cava comes from the liver, clamping the
porta hepatis through the foramen of Winslow with a
noncrushing vascular clamp reduces the blood loss
remarkably. A cavotomy is made adjacent to the
hepatic veins and extended inferiorly to the origin
of the affected renal vein. A 20F Foley catheter with a
30-mL balloon is introduced into the vena cava, and
the balloon is inflated above the level of the thrombus
and withdrawn gently to extract the thrombus out of
the vena cava. In the rare occasion when the tumor
invades the wall of the vein, partial or complete
resection of the vein is considered. Air should be
evacuated from the vena cava before closure. A
Satinsky clamp is applied to the cavotomy, and the
edges of the vena cava are approximated gently with
Allis clamps. The tourniquet on the contralateral renal
vein and infrarenal vena cava and the clamp on the
porta hepatis are released, leaving the tourniquet on
the suprahepatic vena cava in place. The Satinsky
clamp is briefly vented to allow the air in the venal
cava to be evacuated; then the clamp is closed again,
and the last tourniquet on the vein is released. The
affected renal vein is transected flush with the vena
cava. The entire cavotomy is then closed with a
continuous 5-0 polypropylene suture.
Lymphadenectomy
The prognosis of renal cell carcinoma is mostly
affected by presence or absence of nodal metastasis.
Because of the position of the kidney just inferior to
the cisterna chylae, tumor spread from the renal
lymphatic vessels to the cisterna chylae and wide-
spread dissemination of the disease is common.
Curative lymphadenectomy is not possible in most
cases, and the value of lymphadenectomy is limited
to the diagnosis of lymph node involvement. Limited
dissection of the tissue around the junction of the
renal vessel to the nearest great vessel and resection
of the visible or palpable nodes is usually sufficient.
Nephroureterectomy
Transitional cell carcinoma of the calyces, pelvis,
or ureter usually is treated with nephroureterectomy,
provided the contralateral collecting system is normal
and no evidence exists of distant metastasis. Pre-
operative evaluation should include cystoscopy and
bilateral retrograde pyelography for better evaluation
of the collecting system. The operation can be per-
formed through a flank incision with downward
extension, or alternatively two separate incisions or
a midline incision can be made. The technique of
nephrectomy is the same. The ureter is mobilized
with blunt and sharp dissection down to its insertion
in the bladder. A cuff of the bladder must be removed
with the lower ureter because this is the most com-
mon site for tumor recurrence after nephroureterec-
tomy. The bladder is then closed in two layers with
2-0 chromic catgut sutures. A Foley catheter is left in
the bladder for drainage, and a drain in the pelvis
next to the suture line.
Partial nephrectomy
Renal cell carcinoma in a solitary functioning
kidney or bilateral tumors is best treated with partial
R. El-Galley / Radiol Clin N Am 41 (2003) 10531065 1061
nephrectomy. Full preoperative evaluation should be
performed to confirm that the disease is localized.
The arterial anatomy of the affected kidney should be
studied carefully with preoperative angiography.
Flank incisions through the bed of the eleventh or
twelfth rib, with attempt to stay extrapleural and
extraperitoneal, provide an excellent exposure of the
peripheral renal vessels. Then the kidney is mobilized
within Gerotas fascia. Temporary occlusion of the
renal artery and surface cooling of the kidney with
iced slush during the procedure allow 60 minutes of
operating time without significant ischemic injury to
the kidney. For longer procedures the kidney should
be perfused with cold Collins solution through an
arterial catheter, which allows 3 hours for surgery.
Small polar or peripheral renal tumors may not
require renal artery occlusion, however, and the seg-
mental artery instead can be identified and divided.
Simple enucleation for malignant lesions should be
avoided even if the tumor looks well defined, because
of the probable presence of microscopic extensions of
these tumors beyond the pseudocapsule. Tumors of the
upper or lower pole of the kidney are best resected by
polar nephrectomy (guillotine resection), whereas
mid-renal tumors are resected with wedge resection.
Laparoscopic surgery
Over the past few years, laparoscopic surgery has
become more popular than the standard open radical
nephrectomy in many centers and is rapidly becoming
the standard of care in most patients with stage T1 and
T2 tumors (Fig. 8). Laparoscopic surgery offers
smaller cosmetic scars, better visualization, less blood
loss, minimal trauma, and equivalent tumor control to
open surgery, which is reflected in reduced morbidity
and increased patient satisfaction [24]. The contra-
indications to laparoscopic surgery include bulky
lymphadenopathy, IVC involvement, and extensive
perinephric visceral involvement. Unlike laparoscopic
radical nephrectomy, the laparoscopic technique for
partial nephrectomy is being developed. The increased
popularity of hand-assisted laparoscopy in the past few
years has reduced the learning curve for many sur-
geons and enabled the surgeons to deal with large
complicated tumors in safe and effective manner
[25,26].
Full laparoscopic radical nephrectomy is per-
formed through three to four laparoscopic ports and
hand-assisted laparoscopy is performed through a
hand port incision (6 to 8 cm) and two to three
instrument ports. The positions for these ports are
variable according the surgeons preference. The
abdomen is insufflated with CO
2
to a pressure of
25 mm hg. The peritoneum is incised at the Toldts
line to mobilize the colon and expose the Gerotas
fascia, which should be kept intact. On the right side,
the duodenum is mobilized medially and the liver is
retracted. The renal pedicle is then dissected and the
ureter is divided. The artery and vein are individually
clamped and divided with a laparoscopic stapler. On
the left side, the spleen and tail of the pancreas should
be mobilized medially by dividing the splenorenal
and splenophrenic ligaments. Then, the kidney is
dissected as on the right side. The kidney is extracted
through the hand port incision if hand-assisted lapa-
roscopy is chosen. If full laparoscopy is used, a
separate incision in the suprapubic area is made for
kidney extraction. Adrenalectomy used to be part of
radical nephrectomy in most patients. More recent
data, however, showed that adrenalectomy is not
necessary for lower pole tumors [2729].
Laparoscopic partial nephrectomy has been a
difficult procedure even for the experienced laparos-
copist. The laparoscopic approach is similar to radical
nephrectomy. After the kidney is dissected, the tumor
is located, preferably with the aid of intraoperative
ultrasound using a laparoscopic probe. The tumor is
then excised with a safety margin. Frozen sections are
obtained to ensure complete resection and hemostasis
is secured with electrocautery, fibrin glue, or sutures.
If the collecting system is opened, it should be closed
with water-tight sutures. The most difficult part of this
procedure is obtaining hemostasis. Desai et al [30]
have suggested a technique similar to open partial
nephrectomy. The kidney is dissected, the renal vessels
are dissected and clamped with laparoscopic Pull Dog
clamps, and the kidney is cooled with ice slush before
excising the tumor area.
An alternative to partial nephrectomy for small
renal tumors is the destruction of the tumor area with
freezing or radiofrequency ablation. These techniques Fig. 8. Laparoscopic view during radical nephrectomy.
R. El-Galley / Radiol Clin N Am 41 (2003) 10531065 1062
may be performed percutaneously under CT guidance
or laparoscopically. Renal tumor ablation is discussed
elsewhere in this issue.
Results
Local disease control for localized renal tumors is
currently achieved in most patients who were treated
with radical or partial nephrectomy. If the tumor is
completely removed with negative margins, local
recurrence is rare. In most series local recurrence is
reported to occur in less than 2% of patients after
radical nephrectomy [31]. Similarly, in a large series
from Cleveland Clinic, local recurrence was reported
in 3.2% of patients who were treated with partial
nephrectomy; half of these patients had distant me-
tastasis in addition to local recurrence [32,33]. The
cancer-specific survival for patients who were treated
with radical nephrectomy was estimated to be 86.6%,
74%, 68.7%, and 63.8% for 1, 3, 7, and 10 years,
respectively [34]. Local recurrence in the absence of
metastasis is usually amenable to local excision.
Schrodter et al [35] reported on 16 patients who were
diagnosed with local recurrence after radical nephrec-
tomy. At surgical exploration, three patients were
found to have a false-positive CT, whereas the others
had true local recurrence of their tumors. After
complete resection of the recurrence, seven patients
died of metastatic disease after a mean survival of
23 months, and six patients were alive with a mean
follow-up of 53 months [35].
Involvement of the IVC with tumor thrombi occurs
in 4%to 10%of patients. Tumor excision is possible in
most of these patients with a survival range of 77% at
2 years and 55% at 5 years for patients who did have
other evidence of metastasis [36]. Bissada et al [37]
reported on the outcome of the management of renal
cell carcinoma with IVC extension in 54 patients.
Forty-eight patients did not have evidence of other
metastasis. Seven patients had invasion of the IVC
wall and required partial or complete resection of the
IVC. Of the 48 patients without evidence of metastasis
at surgery, the perioperative mortality rate was 2%.
Twenty-two patients (47%) were alive without evi-
dence of metastases, 4%developed solitary metastasis,
and 36% eventually developed multiple metastases.
The follow-up ranged from 25 to 144 months.
It is generally accepted that patients with lymph
node metastasis have a poor prognosis regardless of
the completeness of lymphadenectomy [38,39]. The
reported incidence of lymph node metastasis in renal
cancer patients is 13% [40]. The 5- and 10-year
survival for patients with renal cell carcinoma and
lymph node metastasis is 17% and 5%, respectively
[41]. Minervini et al [42] compared the survival for
renal cell carcinoma patients who had regional lym-
phadenectomy compared with patients who were
managed by radical nephrectomy alone. The 5-year
overall survival was similar whether or not lympha-
denectomy was performed: 79% for radical nephrec-
tomy alone and 78% for radical nephrectomy and
regional lymphadenectomy.
Since the introduction of laparoscopic radical and
total nephrectomy for renal tumor in June 1990, it has
been applied successfully worldwide to hundreds of
patients [43]. Recent data have shown this procedure
to produce cancer control identical to that of open
radical and total nephrectomy [44]. Although in most
centers the cost of the procedure remains higher than
open surgery, the patient benefits of decreased pain,
reduced hospitalization, less blood loss, and more
rapid convalescence seem to be universal [45]. At this
time, laparoscopic radical and total nephrectomy for
the treatment of renal tumors should become the new
standard of care in many centers [46].
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Percutaneous image-guided radiofrequency ablation
of renal malignancies
Ronald J. Zagoria, MD
Department of Radiology, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem,
NC 284011088, USA
The treatment of renal cell carcinoma (RCC) can
be a vexing problem. Although advanced disease
does not respond well to therapy and the prognosis
remains extremely poor, the rate of RCC diagnosis
has increased substantially [1]. In the year 2002, there
were over 30,000 new cases of RCC diagnosed in the
United States [2]. This equates to greater than a 100%
increase in the incidence of RCC diagnosed in the
United States since 1950. Most of this increase has
occurred because of the diagnosis of small, localized
tumors detected incidentally in asymptomatic patients
imaged for other reasons [3].
Radical nephrectomy has long been considered
the standard treatment for localized RCC. Mean-
while, renal-sparing surgery has grown in popularity
and the techniques have been refined. Studies com-
paring surgical techniques have shown that open
partial nephrectomy is as effective in curing small,
localized RCCs as radical nephrectomy [4,5]. This
indicates that complete eradication of a renal tumor
can result in cure rates comparable with those of
treatment using complete removal of a kidney con-
taining a tumor. Advances in imaging and thermal
ablation techniques, combined with the theory that
tumor destruction yields results comparable with
tumor resection, have led to increased interest in
image-guided, minimally invasive percutaneous ther-
mal ablative techniques for the treatment of RCC.
There is substantial experience in treatment of neo-
plasms using both radiofrequency ablation (RFA)
[69], which causes tumor destruction by heating,
and cryotherapy, which destroys tumors using freez-
ing [1013]. Most cryotherapy devices require a
sizeable portal to introduce the ablation device.
Cryotherapy usually requires laparoscopic or open
surgery. Although radiofrequency devices can be
introduced intraoperatively during an open procedure,
most experience with this technique has used percu-
taneous image-guided procedures.
Radiofrequency ablation uses the introduction of a
high-frequency, alternating current within the targeted
tissue [7]. Emission of this energy in a patient to
whom grounding pads have been applied results in
concentrated ionic agitation in tissues nearby the site
of energy transmission. This ionic agitation in turn
results in the generation of heat. This type of thermal
ablative technique is akin to microwave heating used
in everyday applications. When living human tissues
are heated above 49C immediate cell death occurs
[14]. The cell death is induced by denaturation of
protein, melting of cell membranes, and thermal
destruction of cytoplasm [14]. This results in direct
cytodestruction of the affected cells. Some cells are
destroyed at temperatures below 49C, but some cells
can survive temperatures approaching 49C. For per-
cutaneous image-guided RFA the energy is delivered
into the target tissue through needle-shaped probes.
Currently available RFA electrodes range in diameter
from 15 to 17 gauge. Three radiofrequency devices
approved by the Food and Drug Administration are
available in the United States. Each of these uses a
different strategy to maximize the size of thermal
ablation. Each device also uses a slightly different
approach to energy delivery for thermal destruction.
All of the available radiofrequency devices use genera-
tors that deliver between 150 and 200 W of energy.
This represents an increase over earlier generators that
delivered 50 to 125 W of energy. This lower energy
proved suboptimal. The next generation of radio-
0033-8389/03/$ see front matter D 2003 Elsevier Inc. All rights reserved.
doi:10.1016/S0033-8389(03)00074-5
E-mail address: rzagoria@wfubmc.edu
Radiol Clin N Am 41 (2003) 10671075
frequency generators may deliver even higher levels of
energy to increase the area of the treatment zone.
The maximum size of the treatment zone for in
vivo treatment of renal tumors has been shown to
approximate a 5 cm sphere for a single RFA [7]. The
size of the zone of ablation is often smaller than this
maximum, and usually averages between a 3- and
4-cm sphere [14]. The maximum size of the treatment
zone is increased by inducing ischemia, or in devas-
cularized tissue. Alternatively flowing blood, large
fluid-containing spaces, or circulating air can de-
crease the effective size of the treatment zone [14].
When RFA of renal tumors is performed using a
percutaneous technique, imaging guidance is required.
This is usually done using CTscanning or sonography.
The technique of placing the electrode is analogous to
R.J. Zagoria / Radiol Clin N Am 41 (2003) 10671075 1068
that of performing an image-guided biopsy of a renal
mass (Fig. 1). The actual treatment of the tumor can be
quite painful; more sedation is required than for a
standard needle biopsy. Most cases are performed with
conscious sedation and local anesthesia [7].
Percutaneous RFA has been applied for the pri-
mary treatment of RCC in nonoperative patients
[6,8,9], for the treatment of local recurrences of
RCC that are deemed inoperable [15], and also for
the treatment of isolated metastases from RCC
primaries [1]. At the authors institution they per-
formed a phase two clinical trial using the in vivo
application of RFA of renal parenchymal tumors
immediately before nephrectomy [7]. Biopsies were
obtained of all tumors before RFA. The ablation was
performed intraoperatively using ultrasound guidance.
In this study, a Radionics cool-tip radiofrequency
system (Radionics, Burlington, MA), which consists
of the CC-1 Cosman Coagulator, the cool-tip treatment
electrode, and a peristaltic perfusion pump, was used.
Following tumor biopsy a single RFA of 12 minutes
duration was performed using the automatic output
control setting of this radiofrequency generator. Fol-
lowing the single RFA a nephrectomy was performed
and the tumor was evaluated histologically using both
standard and vital stains.
The tumors treated in this study were all deter-
mined to be RCCs (nine clear cell carcinomas and
one papillary carcinoma). The tumors ranged in size
from 1.4 to 8 cm in diameter. The average tumor size
in this series was 3.2 cm in diameter. Eight of the
10 tumors were completely destroyed with no identi-
fiable viable tumor remaining after a single 12-minute
ablation. Two tumors, 1.4 and 8 cm in diameter,
were incompletely treated with a single ablation. The
1.4-cm tumor had approximately 70% destruction but
the temperature in the tissue immediately following the
ablation was below the target temperature of 49C or
higher. A large segment of the 8-cm tumor was
destroyed with viable tumor remaining at the periph-
ery. In all cases no skip areas of viable tumor were
identified in the necrotic regions. Evaluation of the
surrounding kidney following nephrectomy demon-
strated that a margin of treated, nonviable kidney tissue
was identified in all eight of the completely ablated
tumors. The treatment margin ranged from 2 to 13 mm
in thickness. In no case was the rim of destroyed
normal kidney greater than 13 mm in diameter.
The results of this study are encouraging and indi-
cate that in vivo treatment of small RCCs is feasible,
although clearly some tumors require greater than
one 12-minute RFA treatment for complete destruc-
tion of the tumor. Based on this study it seems that
only a small amount of adjacent normal kidney is
destroyed, suggesting that little diminution in renal
function results when using this technique.
In 1992, the first published report using radio-
frequency tissue ablation was released. This used
RFA for the treatment of hepatic tissues [16]. In
1997, the use of RFA to produce extensive necrosis
of kidney tumors in humans was reported [17]. In
1998, a case report was published reporting the first
case where percutaneous RFA was used for the
complete treatment of an RCC in a human under
ultrasound guidance [18].
Since those reports were published, several other
larger studies using RFA for the treatment of renal
tumors have been published [69]. One group has
used RFA ablation in a porcine model and found that
RFA of renal tumors results in necrosis of the ablated
tumor and surrounding renal parenchyma with no
evidence of collecting system damage [19]. One
group has reported their experience treating nine
renal tumors in eight patients using percutaneous
RFA [6]. With a follow-up of just over 10 months
in these eight patients, seven of the nine tumors were
completely free of demonstrable enhancement on CT
scans suggesting complete ablation of these seven
tumors. Within this group of tumors, five of five
exophytic tumors were rendered completely non-
enhancing, whereas only one of three central RCCs
was completely free of enhancement on follow-up
Fig. 1. The technique of radiofrequency ablation (RFA) of renal malignancies in an elderly man with multiple co-morbidities and
an enlarging biopsy-proved renal cell carcinoma (RCC). (A) Unenhanced CT shows the 3-cm RCC (arrow) extending from the
upper pole of the right kidney. This measured 22 HU on this scan. (B) Following contrast material injection this tumor enhanced
to 99 HU on this scan obtained several months before the ablation procedure. (C) CT scan obtained during the RFA procedure
shows the patient in a prone position with the percutaneous radiofrequency electrode (arrow) placed so the tip is bisecting the
tumor. There is a small amount of blood (arrowhead) in the perinephric space, a common finding seen during this procedure. A
22-gauge needle is seen adjacent to the electrode. This was used to target the tumor using a tandem technique. (D) An
unenhanced CT scan obtained 14 months after the ablation shows the ablated RCC is slightly hyperdense compared with the
kidney. It measured 33 HU on this scan. There is a small amount of perinephric stranding seen adjacent to the kidney, an
expected finding following percutaneous RFA. (E) Following contrast material injection the mass shows no enhancement
measuring 35 HU. Lack of enhancement and stability of the tumor size strongly suggests complete tumor destruction.
R.J. Zagoria / Radiol Clin N Am 41 (2003) 10671075 1069
CT. All three RCCs smaller than 3 cm were rendered
completely nonenhancing, whereas four of six RCCs
greater than 3 cm were completely ablated. These
authors reported that multiple ablations within a
single treatment session, or repeated treatment ses-
sions, are often needed to destroy RCCs completely,
particularly those located centrally. Although micro-
scopic hematuria was common in the 24-hour period
immediately following ablation there were no serious
complications in any of these eight patients.
In one larger series 24 RCCs in 21 patients with
von Hippel-Lindau disease or with familial papillary
Fig. 2. MR imaging of an RCC before and after percutaneous RFA showing residual viable tumor requiring repeat ablation.
(A) T1-weighted MR image before gadolinium injection shows the 3-cm RCC arising from the upper pole of the right kidney.
(B) T1-weighted MR image at the same level following gadolinium injection shows marked heterogeneous enhancement of the
tumor. (C) CT scan obtained during the RFA procedure shows the patient in a prone position with the percutaneous
radiofrequency electrode (arrow) placed so the tip is bisecting the tumor in the right kidney. There is a small amount of blood
(arrowhead) in the perinephric space from this procedure. (D) T1-weighted MR image before gadolinium injection obtained
4 months after the percutaneous renal tumor ablation shows heterogeneous increased signal in much of the tumor. This is
commonly seen and is believed caused by coagulative necrosis in the ablated tumor. (E) Following gadolinium injection this
T1-weighted MR image with fat saturation shows a small area of enhancement (arrows) in the anterior aspect of the otherwise
nonenhancing tumor. This enhancement was interpreted as an area of residual viable tumor. The perinephric hemorrhage that
occurred during the ablation is again seen. ( F) CT scan obtained during the second RFA procedure shows the patient in a prone
position with the percutaneous radiofrequency electrode (arrow) placed so the tip is located in the area where viable tumor was
demonstrated on the MR image shown in Fig. 2E. ( G) This T1-weighted MR image with fat saturation and following gadolinium
injection was obtained 4 months after the second percutaneous ablation. No enhancement was detectable within the treated tumor
suggesting complete tumor destruction.
R.J. Zagoria / Radiol Clin N Am 41 (2003) 10671075 1070
RCCs were treated with percutaneous RFA [8]. At a
2-month follow-up, 19 of the 24 treated tumors
demonstrated no evidence of contrast enhancement
on CT imaging. The remaining five tumors demon-
strated some persistent enhancement. There were no
serious complications in this series of patients and all
of these patients were treated on an outpatient basis.
Contrast-infused CT and MR imaging have been
used to detect viable tumor following renal tumor
RFA. In one in vivo study there were no skip areas
where viable tumor survived within the ablation zone
[7], so these should be reliable methods for following
these patients. In a second in vivo study using a
different RFA device, however, 5% to 10% viable
tumor remained in most tumors [20]. This group also
found that contrast enhancement could not always be
detected with CT in areas where viable tumor was
histologically demonstrated following nephrectomy
[20]. This suggests the possibility that lack of contrast
enhancement may overestimate tumor destruction
caused by RFA.
In many cases coagulative necrosis within the
treated area often has a higher baseline attenuation
and high signal on T1 and T2 sequences when
imaged with CT or MR imaging, respectively
(see Fig. 1; Fig. 2). This should not be misinterpreted
as viable neoplasm. Areas of enhancement should be
viewed, however, as residual viable tumor and re-
treated (see Fig. 2).
There is a growing body of knowledge regarding
percutaneous RFA of RCCs. It seems this technique
has a low complication rate, preserves renal function,
is well tolerated by patients, and can result in com-
plete destruction of renal tumors 5 cm or smaller in
most patients (Fig. 3). In some patients viable tumor
can be demonstrated following one session of RFA
(see Fig. 2). This may require further ablation ses-
sions (see Fig. 2). Repeated RFA ablations have been
performed in many patients with renal tumors [6] and
routinely in patients with hepatic tumors, where RFA
experience is more extensive than in the kidney.
Repeat RFA for treatment of residual tumor seems
Fig. 2 (continued).
R.J. Zagoria / Radiol Clin N Am 41 (2003) 10671075 1071
to be a safe procedure without a risk greater than with
primary RFA. It seems that there is little renal damage
associated with RFA. Even in the treatment of central
tumors the development of clinically important pel-
vicalyceal damage has not been reported. Because in
vivo studies have demonstrated only a small amount
of kidney destruction in the area surrounding the
tumor, renal function should remain nearly intact
following this procedure. Obviously, there is limited
information on this procedure and at this time it
should be reserved for patients for whom some
treatment is indicated, but who are not surgical
candidates. Long-term results for this procedure have
yet to be reported.
Radiofrequency ablation also has been used for
other applications in treating RCCs. A single case
report described the successful use of RFA to treat
intractable gross hematuria resulting froma large RCC
[21]. In this case, the life-threatening hematuria failed
to resolve following standard techniques including
renal embolization therapy. RFAwas performed with-
out complications and the patient remained free of
hematuria for a prolonged period of time. In this case,
RFA was used for palliation of symptoms from RCC
rather than as a curative technique.
Radiofrequency ablation also has been used for
the treatment of recurrent and metastatic RCC. There
have only been anecdotal successes reported; this
technique must be viewed as preliminary, but prom-
ising. At the authors institution they have used RFA
to treat unresectable local recurrence from RCC in
two patients. In one patient the recurrence was
extremely large and because of impingement on the
neural foramina was debilitating. Extensive RFA
treatment was performed resulting in a marked de-
crease in symptoms and improved quality of life. In
an additional case [15], recurrence of RCC in the
surgical bed occurred (Fig. 4). The recurrence abutted
the abdominal aorta and was believed to be unresect-
able (see Fig. 4). The recurrence was unresponsive to
immunotherapy and chemotherapy and continued to
grow during CT surveillance monitoring. A single
session of percutaneous CT-guided RFA was per-
formed on this recurrent tumor (see Fig. 4). An
immediate contrast-infused CT demonstrated no evi-
dence of complications. No enhancing tumor could
be demonstrated immediately following the RFA
treatment. This patient has remained free of identifi-
able disease (see Fig. 4) for over 16 months [15]. The
treated area of recurrence has decreased in volume
with no evidence of enhancing, viable tumor. In these
two cases RFA seemed to be helpful in the treatment
of locally recurrent RCC. This is a very promising
area for the use of image-guided RFA therapy.
In addition, in some cases patients with distant
metastases from RCC may experience prolonged
survival with eradication of the metastases [22]. This
well-documented phenomenon has most often been
seen in patients following metastasectomy of a small
number of pulmonary metastases from RCC [22]. In
general, patients with metastatic RCC have an ex-
tremely poor prognosis with nearly no 5-year sur-
vivals following diagnosis [23]. Metastatic RCC is
nearly always incurable with systemic immuno-
therapy or chemotherapy. Even though some case
reports show prolonged tumor remission following
metastasectomy, surgical resection of pulmonary
metastases uncommonly results in improved progno-
Fig. 3. Successful ablation of a larger, centrally located RCC. (A) Unenhanced CTscan shows a 5 cm3 cmtumor (arrow) located
centrally in the left kidney. (B) Contrast-enhanced CTobtained immediately following percutaneous ablation shows heterogeneity
of the treated tumor without enhancement. There is perinephric hemorrhage present resulting from the ablation procedure.
R.J. Zagoria / Radiol Clin N Am 41 (2003) 10671075 1072
sis for RCC patients [22]; surgeons are often reluc-
tant to perform this procedure. This may be another
opportunity for the use of image-guided percutane-
ous RFA treatment. In one published report a patient
with two pulmonary metastases from a previously
resected RCC was successfully treated with percuta-
neous CT-guided RFA [24]. In this patient, the two
pulmonary metastases were peripherally located in
the right lower lobe of the lung (Fig. 5). At 18-month
follow-up, this patient has not received any other
treatment for his RCC, but remains free of detectable
disease (see Fig. 5). The use of image-guided RFA
for treatment of isolated metastases from RCC as in
this reported case is promising, but at this point it
should be reserved as a last resort in nonoperative
candidates until larger studies can demonstrate its
efficacy compared with surgery. Percutaneous RFA
has been used to treat neoplasms in sites where RCC
commonly metastasizes, however, including the
lungs, liver, and the skeleton. The morbidity associ-
ated with this type of treatment based on experience
with other neoplasms in these locations is very low
with serious complications occurring in less than 5%
of treated patients [25]. Because of the low morbidity
and extremely low risk of mortality associated with
image-guided percutaneous RFA, this treatment may
Fig. 4. Percutaneous radiofrequency of a recurrent RCC. (A) Contrast-enhanced CT scan shows an enhancing mass (arrow)
abutting the aorta and the superior mesenteric artery in this man who previously had a left nephrectomy for RCC. A biopsy of
this mass was found to be recurrent RCC. (B) CT scan obtained during the RFA procedure shows the patient in a prone position
with the percutaneous radiofrequency electrode (arrow) placed so the tip is bisecting the tumor. This scan also shows a small
amount of gas in the tumor adjacent to the electrode. This common finding is attributable to necrosis and vaporization of tissue
induced by the radiofrequency energy. (C) Contrast-enhanced CT scan obtained 10 months after the ablation procedure shows
that tumor has decreased in size and no enhancement, consistent with complete tumor destruction. The superior mesenteric artery
and aorta remain widely patent.
R.J. Zagoria / Radiol Clin N Am 41 (2003) 10671075 1073
be considered for patients who have failed systemic
therapy, and in whom the potential benefits of
surgery seem to be outweighed by the risk of
substantial morbidity resulting from successful me-
tastasis resection.
Summary
There is a growing body of experience supporting
the use of image-guided RFA for the treatment of
primary RCC. Because surgical resection is a tech-
nique with low mortality, and a proved success rate
that is high, this must remain standard therapy for
patients with potentially curable RCC. Some patients
with low-stage RCC, however, may not be surgical
candidates. Image-guided RFA is an option for treat-
ment of these patients. In addition, image-guided
RFA shows promise for the successful care of other
patients with RCC. In particular, RFA has been used
successfully for the treatment of intractable hematuria
resulting from an RCC; local recurrences of RCC,
both for attempted cure and for palliation of symp-
toms; and finally for the treatment of isolated metas-
tases from RCC. As with the treatment of primary
RCC, the data remain limited for these applications.
Fig. 5. Percutaneous RFA of pulmonary metastasis from RCC. (A) CT shows one of two pulmonary metastases in this patient
with a history of RCC. These biopsy-proved metastases were refractory to systemic therapy. (B) CT scan obtained during the
RFA procedure shows the patient in a prone position with the percutaneous radiofrequency electrode placed so the tip is bisecting
the tumor in the right lung. (C) CTscan obtained 29 months after the ablation procedure shows a small area of scarring where the
tumor had been located. There was no evidence of viable tumor in either of the treated lung metastases.
R.J. Zagoria / Radiol Clin N Am 41 (2003) 10671075 1074
This technique should be reserved until after standard
therapies have been exhausted. It seems likely that
some form of image-guided percutaneous tumor
therapy, such as RFA, will become an alternative
treatment modality in some patients with potentially
curable RCC.
References
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R.J. Zagoria / Radiol Clin N Am 41 (2003) 10671075 1075
Index
Note: Page numbers of article titles are in boldface type.
A
Acceleration index, in color Doppler imaging, in
infants, 933934
ACE inhibitor renal scintigraphy, of hypertension, in
infants, 939941
of renal artery stenosis, 913914
Aneurysms, renal artery, and hypertension, 922923
Angiography, CT. See CT angiography.
intra-arterial, of renal artery stenosis, 919
MR. See MR angiography.
of hypertension, in infants, 935937
of renal trauma, 1019
Angiomyolipomas, imaging of, ultrasound contrast
agents in, 963965
Angioplasty, for renal artery stenosis, 919, 921
Arteriography, intra-arterial digital subtraction, of
hypertension, in infants, 936
Arteriovenous communications, and hypertension,
923924
Atherosclerotic disease, and renal artery stenosis, 911
B
Birt-Hogg-Dube syndrome, imaging of, 10441045
Breathhold imaging, of kidneys, 880, 882
C
Calcifications, renal, CT of, 867
Captopril, in MR imaging, of renal function,
10061008
Catheter-associated thromboembolism, angiography
of, in infants, 937
ultrasonography of, in infants, 933
Chromosome 3, translocation of, and hereditary renal
cancer, 1046
Color Doppler imaging, of hypertension, in infants,
933935
Computed tomography, of kidneys. See Kidneys.
of renal trauma. See Renal trauma.
of urinary lithiasis. See Urinary lithiasis.
of von Hippel-Lindau disease, 1040
Contusions, renal, imaging of, 10261027
Crossing vessels, renal, CT of, 871
Cryotherapy, for von Hippel-Lindau disease,
10401041
CT angiography, of hypertension, in infants, 941
of kidneys, versus CT, 866867
of renal artery stenosis, 918919
of renal masses, 870871
CT urography, of hematuria, 944, 946953
technique for, 944, 946953
excretory-phase CT with multiplanar
reformation, 951953
scanned projection radiographic
technique, 948
Cyclosporine toxicity, and renal transplant
dysfunction, MR imaging of, 1013
Cystic masses, renal, imaging of, ultrasound contrast
agents in, 965968
ultrasonography of, in infants, 932
D
Diabetic nephropathy, and hypertension, 925
Diagnostic peritoneal lavage, for renal trauma, 1020
Dissection, renal artery, and hypertension, 923
Doppler ultrasonography, of renal artery stenosis,
914, 916917
0033-8389/03/$ see front matter D 2003 Elsevier Inc. All rights reserved.
doi:10.1016/S0033-8389(03)00131-3
Radiol Clin N Am 41 (2003) 10771082
F
Familial renal cancer, imaging of, 1046
Familial renal oncocytomas, imaging of, 1045
Fibroids, uterine, hereditary leiomyoma renal cell
carcinoma and, 1043
Fibromuscular dysplasia, and renal artery stenosis,
911912
G
Glomerular filtration rate, MR imaging of,
10041006
Glomerulonephritis, and hypertension, 924925
Gray-scale ultrasonography, in infants, 932933
H
Harmonic imaging, of kidneys, 962
Hematomas, perinephric, imaging of, 1027
subcapsular, and hypertension, 926927
imaging of, 1027
Hematuria, CT of, 867
CT urography of. See CT urography.
MR urography of. See MR urography.
radiofrequency ablation of, 1068
Hereditary renal cancer, 10351049
Birt-Hogg-Dube syndrome, 10441045
familial renal cancer, 1046
familial renal oncocytomas, 1045
histologic subtypes of, 1035, 1037
leiomyoma renal cell carcinoma, 10421043
medullary carcinoma, 1045
papillary renal carcinoma, 10411042
translocation of chromosome 3, 1046
tuberous sclerosis, 1046
von Hippel-Lindau disease, 10371041
cryotherapy for, 10401041
CT of, 1040
MR imaging of, 1040
nephron-sparing surgery for, 1040
radiofrequency ablation of, 10401041
Hydronephrosis, MR urography of, 10081009
Hypertension, in infants, 929942
angiography of, 935937
CT angiography of, 941
diagnosis of, clinical aspects of, 929930
imaging of, etiology and, 931
nuclear medicine studies of, 937941
ultrasonography of, 931935
renal causes of, 909928
arteriovenous communications, 923924
chronic pyelonephritis, 925926
diabetic nephropathy, 925
evaluation of, 927
glomerulonephritis, 924925
midaortic syndrome, 922
nephroslcerosis, 925
neurofibromatosis, 921922
polyarteritis nodosa, 923
polycystic kidney disease, 926
posttraumatic stenosis, 924
renal artery aneurysm and dissection, 922923
renal artery stenosis, 909914, 916919, 921
ACE inhibitor renal scintigraphy of,
913914
atherosclerotic disease in, 911
CT angiography of, 918919
Doppler ultrasonography of, 914, 916917
fibromuscular dysplasia in, 911912
functional versus anatomic imaging of, 913
intra-arterial angiography of, 919
management of, 919, 921
MR angiography of, 917918
subcapsular hematomas, 926927
Takayasua arteritis, 921
tumors, 926
I
Infarctions, renal, imaging of, 1028
ultrasound contrast agents in, 971972
Intra-arterial angiography, of renal artery
stenosis, 919
Intra-arterial digital subtraction arteriography, of
hypertension, in infants, 936
Intravenous urography, of renal trauma, 1018
J
Juxtaglomerular cell tumors, and hypertension, 926
K
Kidneys, CT of, 863875
compression for distention in, 874
contrast in, 864866
concentration and total dosage, 864865
high-concentration contrast, 865866
Index / Radiol Clin N Am 41 (2003) 10771082 1078
injection rates, 865
oral contrast versus water, 865
detectors in, 864
for crossing vessels, 871
for renal masses, 868871
characterization of, 869
delayed imaging in, 870
nephrographic phase in, 870
staging of, 869870
versus CT angiography, 870871
for transplant donor evaluation, 871
for trauma, 868
for urolithiasis, 867868
molecular imaging in, 874
pitch in, 863864
radiation dosage in, 872873
in children, 872, 873
in pregnancy, 872873
reconstruction in, 864
versus CT angiography, 866867
volumetric acquisition in, 873874
devascularized, imaging of, 1030
imaging of, ultrasound contrast agents in.
See Ultrasound contrast agents.
MR imaging of, 877907
breathhold technique for, 880, 882
contrast-enhanced dynamic imaging, 895898
applications of, 895898
contrast media and volume in, 898
contrast rate in, 898
flush volume and rate in, 898
power injector in, 898
timing of, 898
flow-sensitive imaging, 894895
for renal arteries, 878880
versus MR angiography, 878880
for renal masses, 877878
for renal veins, 880
for urothelial tumors, 878
image processing in, 898, 900901
subtraction in, 898, 900
three-dimensional reconstruction in,
900901
non-breathhold technique for, 882884
coils and parallel imaging in, 883884
fast acquisitions in, 882883
motion compensation strategies in, 883
T1-weighted imaging, 886888, 890894
applications of, 886
gradient-echo sequences in, 886888
in-phase and opposed phase, 888, 890891
spin-echo sequences in, 892
three-dimensional, 892894
two- versus three-dimensional, 892
T2-weighted imaging, 884886
applications of, 884
echo-train imaging in, 885886
Half-Fourier reconstruction in, 886
spin echo sequences in, 884885
shattered, imaging of, 10281029
L
Lacerations, renal, imaging of, 1027
Laparoscopic nephrectomy, for renal tumors,
1060, 1061
Leiomyoma renal cell carcinoma, hereditary, imaging
of, 10421043
Leiomyomas, malignant potential of, 1043
Leiomyosarcomas, malignant potential of, 1043
Lithiasis, urinary. See Urinary lithiasis.
Lymphadenectomy, for renal tumors, 1059, 1061
M
Magnetic resonance imaging, of kidneys.
See Kidneys.
of renal function. See Renal function.
of renal trauma, 1021
of urinary lithiasis, versus CT, 988, 990
of von Hippel-Lindau disease, 1040
Medullary carcinoma, imaging of, 1045
Metastatic disease, from renal cell carcinoma,
radiofrequency ablation of, 10681070
Midaortic syndrome, and hypertension, 922
Molecular imaging, of kidneys, 874
MR angiography, of renal arteries, 878880
of renal artery stenosis, 917918
three-dimensional, of kidneys, 892894
MR urography, of hematuria, 953957
gadolinium-enhanced T1-weighted, 955957
heavily T2-weighted, 953955
of hydronephrosis, 10081009
N
Nephrectomy, partial, for renal tumors, 10591061
laparoscopic, for renal tumors, 1060, 1061
radical, for renal tumors, 10571058, 10601061
laparoscopic, for renal tumors, 1060, 1061
Index / Radiol Clin N Am 41 (2003) 10771082 1079
Nephron-sparing surgery, for von Hippel-Lindau
disease, 1040
Nephropathy, diabetic, and hypertension, 925
Nephrosclerosis, and hypertension, 925
Nephroureterectomy, for renal tumors, 1059
Neurofibromatosis, and hypertension, 921922
Non-breathhold imaging, of kidneys. See Kidneys,
MR imaging of.
Nuclear medicine studies, of hypertension, in infants,
937941
of renal artery stenosis, 913914
of renal trauma, 1021
O
Oncocytomas, familial renal, imaging of, 1045
P
Papillary renal carcinoma, hereditary, imaging of,
10411042
Partial nephrectomy, for renal tumors, 10591061
laparoscopic, for renal tumors, 1060, 1061
Percutaneous transluminal renal artery angioplasty,
for renal artery stenosis, 919, 921
Perinephric hematomas, imaging of, 1027
Phleboliths, versus urinary lithiasis, 980, 982983
Plain films, of renal trauma, 1018
Polyarteritis nodosa, and hypertension, 923
Polycystic kidney disease, and hypertension, 926
Posttraumatic stenosis, of renal artery, and hyperten-
sion, 924
Pregnancy, radiation dosage in, 872873
Pseudotumors, renal, imaging of, ultrasound contrast
agents in, 968
Pyelography, retrograde, of renal trauma, 1020
Pyelonephritis, chronic, and hypertension, 925926
imaging of, ultrasound contrast agents in,
972973
R
Radical nephrectomy, for renal tumors, 10571058,
10601061
laparoscopic, for renal tumors, 1060, 1061
Radiofrequency ablation, of renal cell carcinoma. See
Renal cell carcinoma.
of von Hippel-Lindau disease, 10401041
Renal arteries, MR imaging of, 878880
Renal artery aneurysms, and hypertension,
922923
Renal artery dissection, and hypertension, 923
Renal artery stenosis, and hypertension.
See Hypertension.
imaging of, ultrasound contrast agents in, 971
Renal artery thrombosis, ultrasonography of, in
infants, 932
Renal cancer, hereditary. See Hereditary
renal cancer.
Renal cell carcinoma, imaging of, ultrasound contrast
agents in, 963
radiofrequency ablation of, 10631071
clinical studies of, 10651067
devices for, 10631064
for distant metastases, 1068-1070
for recurrent disease, 1068
treatment zone in, 1064
tumor size and, 1065
viable tumor following, 1067
Renal cystic diseases, ultrasonography of, in
infants, 932
Renal function, MR imaging of, 9991015
captopril in, 10061008
contrast quantification in, 10001001
for hydronephrosis, 10081009
for renal transplant evaluation, 10091013
gadolinium dose optimization in, 1001
glomerular filtration rate in, 10041006
image postprocessing in, 10011002
perfusion imaging in, 10021004
arterial spin labeling technique for, 1003
blood oxygen level-dependent imaging in,
10031004
extravascular contrast agents in, 10021003
intravascular contrast agents in, 1003
Renal masses, CT of. See Kidneys, CT of.
cystic, imaging of, ultrasound contrast agents in,
965968
indeterminate, imaging of, ultrasound contrast
agents in, 969, 971
MR imaging of, 877878
Renal perfusion, imaging of, ultrasound contrast
agents in, 971973
Index / Radiol Clin N Am 41 (2003) 10771082 1080
Renal transplantation, donor evaluation for, CT
in, 871
postoperative evaluation of, MR imaging in,
10091013
Renal trauma, classification of, 10241030
grade 1, 10261027
grade 4, 10271028
grade 5, 10281030
grades 2 and 3, 1027
vascular contrast extravasation in, 10303031
imaging of, 10171033
angiography in, 1019
CT in, 868, 10211024
contrast in, 1021
interpretation of, 10231024
technique for, 10211023
diagnostic peritoneal lavage in, 1020
intravenous urography in, 1018
MR imaging in, 1021
nuclear medicine studies in, 1021
patient selection for, 10171018
plain films in, 1018
retrograde pyelography in, 1020
ultrasonography in, 1019
ultrasound contrast agents in, 973
Renal tumors, cystic, 1052
solid, 1052
surgical management of, 10511062
anatomy in, 10521056
blood supply, 10541056
lymphatic drainage, 1056
laparoscopic, 1060, 1061
lymphadenectomy in, 1059, 1061
nephroureterectomy in, 1059
partial nephrectomy in, 10591061
radical nephrectomy in, 10571058,
10601061
surgical approaches in, 1056
vena caval extension and, 10581059
versus pseudotumors, 1052
Renal vein injuries, imaging of, 1030
Renal vein thrombosis, ultrasonography of, in
infants, 932
Renal veins, MR imaging of, 880
Reninomas, and hypertension, 926
Resistive index, in color Doppler imaging, in infants,
933934
Retrograde pyelography, of renal trauma, 1020
S
Sickle cell trait, medullary carcinoma in, 1045
Subcapsular hematomas, and hypertension, 926927
imaging of, 1027
T
Takayasus arteritis, and hypertension, 921
Thromboembolism, catheter-associated, angiography
of, in infants, 937
ultrasonography of, in infants, 933
Thrombosis, renal artery, ultrasonography of, in
infants, 932
renal vein, ultrasonography of, in infants, 932
Trauma, renal. See Renal trauma.
Tuberous sclerosis, and hereditary renal
cancer, 1046
U
Ultrasonography, Doppler, of renal artery stenosis,
914, 916917
of hypertension, in infants, 931935
of renal trauma, 1019
of urinary lithiasis, versus CT, 988
Ultrasound contrast agents, in renal imaging,
961976
intraoperative, 973
microbubble-specific techniques for, 962963
of angiomyolipomas, 963965
of cystic masses, 965968
of indeterminate masses, 969, 971
of infarcts, 971972
of pseudotumors, 968
of pyelonephritis, 972973
of renal artery stenosis, 971
of renal cell carcinoma, 963
of renal perfusion, 971973
of trauma, 973
Ureteral complications, of renal transplantation, MR
imaging of, 1013
Ureteropelvic junction injuries, imaging of,
10291030
Urinary lithiasis, CT of, 977997
advantages and disadvantages of, 977978
interpretation of, 980, 982987
radiation in, 987988
technique for, 978980
versus MR imaging, 988, 990
Index / Radiol Clin N Am 41 (2003) 10771082 1081
versus ultrasonography, 988
versus phleboliths, 980, 982983
Urography, CT. See CT urography.
intravenous, of renal trauma, 1018
MR. See MR urography.
Urolithiasis, CT of, 867868, 872
Urothelial tumors, MR imaging of, 878
Uterine fibroids, hereditary leiomyoma renal cell
carcinoma and, 1043
V
Vena cava, renal tumor extension into, 10581059
von Hippel-Lindau disease. See Hereditary
renal cancer.
Index / Radiol Clin N Am 41 (2003) 10771082 1082