BRIEF CLINICAL OBSERVATIONS

Nondilated Obstructive
Uropathy Due to a
Ureteral Calculus
Aaron Spital, MD, Robert Spataro, MD,
Departments of Medicine and Radiology, University of
Rochester School of Medicine, The Genesee Hospital,

Rochester, New York

ltrasunography has become the standard approach for investigating suspected urinary tract
obstruction because of its safety and high sensitivity.lJ
However, it is important to understand that ultrasonography does not detect obstruction directly, but
rather its usual consequence: dilatation of the renal
collecting system. Unforhmately, urinary tract obstruction is not always accompanied by detectable
dilatation36 In these unusual cases of nondilated obstructive uropathy, the results of conventional ultrasonography will be falsely negative, thereby misleading the physician and possibly delaying diagnosis and
therapy. Most previously reported cases have been the
result of retroperitoneal or pelvic malignancy or fibrosis, or have followed pelvic surgery.56 Here we report a case of nondilated obstructive uropathy caused
by a ureter-al calculus in order to alert physicians to
the possibility that on occasion, even obstruction due
to a urinary stone may be missed by ultrasonography.
While this presentation has been noted previously by
radiologists,5~7-~ it has not been emphasized in the general medical literature.

CASE REPORT
A Wyear-old white male was admitted to The
Genesee Hospital with a Z-day history of intermittent

left-sided flank pain radiating to the groin. His past

medical history included mild renal insufficiency
with a baseline serum creatinine of 1.7 mg/dL, an idiopathic lupus anticoagulant, multiple deep venous
thromboses of the legs, and pulmonary emboli.
Medications
included
coumadin,
vitamins,
and
herbal preparations. On exarntiation the patient was
found to have new hypertension and left-sided abdominal tenderness. Laboratory data revealed a
serum creatinine of 2.5 m@lL and mild microscopic
hematuria. The patient was thought to have renal
colic, although no stone was seen on abdominal
roentgenography.
The following day, a renal ultrasound was obtained
that was completely normal with no evidence of hydronephrosis (Figure IA). Recause of this surprising finding and the history of a hypercoagulable state,
occlusive vascular causes of renal dysfunction were
sought. A radionuclide renal scan showed decreased
blood flow to the left kidney with minimal excretion
and a normal-appearing
right kidney. Selective left
renal arteriography and venography were performed,
but no evidence of vascular obstruction was found.
The patients pain persisted and the serum creatinine remained elevated at 2.3 mg/dL. Therefore, the
renal ultrasound was repeated 3 days after the initial
study. Again, no hydronephrosis
was detected
(Figure 1B). Nonetheless, because of an increasing
index of suspicion for urinary tract obstruction, an
intravenous pyelogram (IVP) was obtained the following day. It showed delayed excretion on the left
side with mild dilatation of the collecting system and
obstruction
at t,he left ureteral vesicle junction
(Figure 2).
On the evening following the IVP, the patient passed
a small stone that was composed of calcium oxalate.

Figure
1A. First ultrasound of the left
kidney
showing
no evidence
of
hydronephrosis.

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BRiEF CLlNlCAL OBSERVATIONS

.,., ._ .,

.,

F@re 13. Second ultrasound of the left kidney again show&

hydronephrosis.

no

The next day, the serum creatinine returned to its previous baseline value of 1.7 mgML. Three weeks later
a repeat radionuclide renal scan was normal

Intravenous pyelography has long been considered the most valuable study for the evaluation of renal colic.277 However, there are several potential complications
of this procedure including
allergic
reactions, contrast-induced renal failure, precipitation of renal colic, and the consequences of exposure to ionizing radiation. In contrast, ultrasonography of the urinary tract is noninvasive and virtually
risk free. Nloreover, some investigators have found
ultrasonography so reliable in the evaluation of renal colic that they have recommended it (rather than
an IS&) as the initial study of choice for the investigation of suspected renal paii~.~,~ However, as the present case illustrates, this approach will occasionally
be misleading.
Our patients initial renal ultrasound was interpreted as being completely normal. Even after the diagnosis had been made j a retrospective review of this
study still failed to show any abnormality. The normal findings on ultrasonography, along with renographic evidence of unilateral poor function and a history of hypercoagulability,
led the physicians to
perform unnecessary invasive procedures to exclude
vascular obstruction as the cause of this patients disorder. A repeat renal ultrasound several days later
was again norm@ but an IVP clearly showed obstruction at the left ureteral vesicle junction.
This unusual presentation of renal calic secondary
to an obstructing stone with no detectable dilatation
on ultrasonography has been previously alluded to
in the radiological literature.1~G~8 In most cases, the
reporting physicians concluded that the obstruction
was very recent and proximal dilatation had not yet
had time to occur. However, our case suggests that
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Figure 2. Thirty-minute oblique radiograph from the intravenous

pyelogram showing blunted fornices with mildly dilated calyces,
renal pelvis, and proximal ureter of the left kidney, consistent
with ureterai obstruction. The right side is normal.

there are other causes of nondilatation

in obstructive nephrolithiasis. Our patient had more than 2 full
days of renal colic before his initial normal sonographic study. The process had been present for 5
days at the time of his second study. These results
are even more impressive when one considers that
the degree of obstruction was severe, as evidenced
by the renographic and urographic findings as well
as the elevation in serum creatinine. The explanation
for this remarkable
presentation
is unknown.
Previously proposed mechanisms include: impaired
peristalsis; for&al
rupture with decompression of
the pelvicalyceal system; atypical anatomy of the collecting system (such as a small intrarenal pelvis)
which resists dilatation; and a severely depressed
glomerular filtration rate secondary to underlying renal disease or volume depletion.1~3-5~BJ0
Regardless of the mechanism, the message is clear.
When a patient presents with renal colic and an obstructing urinary stone is suspected, the physician
should not be dissuaded by negative findings on ultmsonography. In such cases, an IVP should be performed. Indeed, because of the possibility of nondilatation and because the IW can better define the site

BRIEF CLINICAL OBSERVATIONS

and cause of obstruction, many authors still believe

that the IVP is the diagnostic procedure of choice in
t.he evaluation of renal colic.a,g In those rare situations where urography is contraindicated and ultrasonography is normal, retrograde and even antegrade
pyelography should be considered.

REFERENCES
1. Cronan JJ. Contemporary concepts for lmaglng urinary tract obstruction.
UroiRadiol. 1992;14:8-12.
2. Webb JAW. Ultrasonography
In the dlagnosls of renal obstruction. EIMJ.
1990;301:944-946.
3. Gornish M, Lune Y, Wysenbeek AJ. Nondilated obstructive uropathy causing
acute renal failure. Isr J Med SC;. 1990;26:50-52.
4. Lyons K, Matthews P, Evans C. Obstructive uropathy without djlatabon: a
potential dlagnostlc pitfall. BMJ. 1988;296:1517-1518.
5. Malllet PJ, Pelle-Francoz 0, Laville M, et al. NondIlated obstructive acute
renal failure: diagnostic procedures and therapeutic management. Radiology.
1986;160:659-662.
6. Spital A, Valve JR, Segal AJ. Nondilated obstructive uropathy. Urology.
1988:31:478-482.
7. Erwin BC, Carroll BA, Sommer FG. Renal COIIC: the role of ultrasound In initial
evaluation. Radiology. 1984;152:147-150.
8. Haddad MC, Sharlf HS, Shahed MS, et al. Renal colic: dlagnosrs and
outcome. Radiology.
1992;184:83-88.
9. Spencer J, Lindsell 0, Mastorakou
I. Ultrasonography
compared with
Intravenous urography in the investigation of adults with hematurla. BMJ.
1990;301:1074-1076.
10. Platt JF, RubIn JM, EIIIs JH. Acute renal obstruction: evaluation with
lntrarenal duplex doppler and conventional US. Radiology.
1993;186:685688.
Manuscript submltted April 20, 1994
and accepted June 22, 1994.

Trousseaus Syndrome With

Nonbacterial Thrombotic
Endocarditis: Pathogenic
Role of Antiphospholipid
Syndrome
Didier Bessis, MD, Albert Sotto, MD, t!@ital SaintE/o;,Montpellier,Jean-Paul Viard, MD, HbpitalNecker,
Paris, Madeleine Bbard, PhD, HdpitalSaint-Louis,
Paris,Albert-Jean Ciurana, MD, /#pita/ Saint-E/o;,
Montpellier,Marie-Claire Boffa, MD, PhD, &pita/
Saint-Louis,Paris,France

onbacterial thrombotic
endocarditis
(NBTE)
with Trousseaus syndrome is a common manifestation of malignant diseases, particularly in lung,
gastrointestinal,
and pancreatic adenocarcinomas.
The pathophysiologic
mechanisms of these malignancy-associat.ed thromboses are still not clear. We
describe a case of NBTE with Trousseaus syndrome
in a patient with lung adenocarcinoma. The patient
was positive for antiphosphatidylinositol
antibodies
and anti-@ glycoprotzin I (anti-PBGPI) antibodies; to

the best of our knowledge, this combination

never been reported in this pathology.

has

CASE REPORT
July 1992, a previously healthy 48-year-old white
presented with aphasic right palsy that regressed within a few minutes. Five days later, he
complained of severe pain in his left calf and aphasic left facial palsy. Digital subtraction angiography
of the abdominal aorta and lower limbs revealed embolic obliteration of the left tibioperoneal artery. A
cerebral computed tomographic (CT) scan showed
vascular ischemic in&uy of the right temporal and bilateral occipital lobes and t,he left internal capsule.
The patient was given intravenous heparin for I1
days followed by warfarin. One week later, he had a
fever of 38.5C and complained of cramps in his left
leg. A superficial venous thrombosis was noted in the
upper left arm. Venography of the lower limbs revealed thromboses of the bilateral popliteal and tibial veins.
On admission to Hepital Saint-Eloi (Montpellier,
France) 1 month later, the physical examination revealed a systolic murmur in the mitral region and
aphasia with confusional syndrome. The white blood
cell count was 16 X log/L with 68% polymorphonuclear leukocytes. No thrombopenia
or fibrinopenia
was observed. Nine blood cultures were sterile.
Serologic tests for HIV-l and HIV-2, Q fever,
Chlamydia~, Mycoplasma, and Rmtcellu species were
negative. Venereal Disease Research Laboratory test,
Coombs test, rheumatoid factor, antibodies to nuclear components and native DNA, and antineutrophil cytoplasmic autoantibodies were negative.
Lupus anticoagulant
was detected with a prolonged partial activated thromboplastin
time (49 seconds versus 32 seconds for the control), uncorrected
by mixing with normal plasma, and confirmed by
measuring prothrombin time using diluted thromboplastin. The levels of coagulation proteins (factors II,
V, VII, VIII, IX, X, XI, XII), antithrombin
III, protein
C, and protein S were normal.
Antiphospholipid
antibody (aPLA) levels were determined (INSERM U353 and Dr. Pascale Laroche,
Biomedical
Diagnostics, Marne-la-Vallke,
France)
using an enzyme-linked
immunosorbent
assay
(ELISA) on plates coated with different: phospholipids:
cardiolipin,
phosphatidylinositol,
phosphatidylserine,
phosphatidylethanolamine,
either
alone or in combination
(Table). The aPLA levels
were expressed as GPL or MPL units using a standard curve obtained with serially diluted selected
positive sera. Ten unit,s, which corresponded to the
97th percentile of the distribution
of 100 healthy
blood donors, was arbitrarily chosen as the threshold above which aPLA levels were considered to be
In

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