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Alzaiem Al-Azhari University

Faculty of Graduate Studies and Scientific


Research

Estimation of the Frequency of Renal Artery


Stenosis Among Hypertensive Patients Using
Duplex Sonography in Khartoum in 2014

A Thesis Submitted For Partial Fulfillment of the


Requirement of M.Sc Degree in Medical Diagnostic
Ultrasound

Presented By : Dr. Walaa Ismail Musa

Supervisor : Dr. Suzan Omar Abd-Alla


MBBS ( Medicine ), M.Sc (Medical Diagnostic Ultrasound
AAU ), MD ( Diagnostic Radiology SMSB )

2014


)(49

Dedication
To my parents who taught me to help...
To my teachers who made me to know...
To my wonderful friends...

Acknowledgement
A number of people provided comments, help and
moral support,
Special thanks to my supervisor...
Dr Suzan Omar Abd-Alla

Abstract
3

Renal artery stenosis (RAS) is a progressive disease with many


associated morbidities including but not limited to progressive
renal

insufficiency,

hypertension,

myocardial

infarctions,

congestive heart failure, stroke, and death. Early diagnosis of


renal artery stenosis is an important clinical objective because
interventional

therapy

may

improve

or

cure

hypertension,

preserve renal function, and prevent development of end-stage


renal failure.
The aim of this study is to estimate the frequency of renal
artery stenosis among hypertensive patients in Khartoum using
duplex sonography, and to evaluate the relation between renal
artery stenosis and age, gender, and other co morbidities of the
patient.
This study was carried out in Soba University Hospital, Sharq
El-Niel, Khartoum North, and Umdorman Military Hospital, where
100 hypertensive patients were collected randomly from different
ages and different gender, this study has been carried out in 7
months.Duplex ultrasound examination was done on both renal
arteries. Frequency of renal artery stenosis is 2% among studied
cases. , the two affected cases are males, in the age group of 2040 years, with newly discovered hypertention, and no associated
comorbiditiy, no other kidney sonographic abnormality, one of
them has normal renal function test and the other has abnormal
test.

The study emphasized the role of duplex sonography as a


screening and diagnosis tool for renal artery stenosis and the
importance of early scanning. It recommends to improve the local
practice of renal artery duplex by following the universal protocols
and continuous training and machines quality assurance.


) (RAS



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100

7
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2
40-20


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Page
No
I
II
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Contents

Dedication
Acknowledgements
6

No
1

2
3

4
5
6
7
8
9

Abstract(English)
Abstract (Arabic)
Table of contents
List of abbreviations
List of tables
List of figures

IV
V
VI
VII
IX
XI
Chapter One

1-1
1-2
2-1
2-2
2-3
2-4
2-5
2-6
2-7
2-8
2-9
3
4
5-1
5-2
5-3

Introduction
Objectives

1
4

Chapter Two
Historical Background
Renal Circulation Anatomy & Physiology
Etiology of Renal Artery Stenosis
Pathophysiology of Renovascular Hypertension
Clinical Clues of Renovascular Hypertension
Screening Tests
Therapy of Renovascular Hypertension
Duplex Ultrasound of the Renal Artery
Background Comparative studies
Chapter Three
Material &Methodology
Chapter four
Results
Chapter Five
Discussion
Conclusion
Recommendations
References
Appendix

4
5
8
9
10
11
17
19
25
27
30
56
58
59
60
62

Abbreviations
ACE angiotensin converting enzyme

ACEI

angiotensin converting enzyme

ARB

inhibitor

angiotensin receptor blocker


7

AP
CT
DPTA

arterial pressure

computed tomography

diethylenatriaminepentacetic acid

DSA

digital substraction angiography


EDV
ESRD
FMD

end diastolic velocity


end stage renal failure
fibromuscular dysplasia

IVP

intravenous pyelography

MAG3 mercaptoacetyltriglycerin
MIP
MRA

maximum intensity projection

magnetic resonance angiography


OM
PRA

outer medulla

plasma rennin average

PTRA percutaneous transluminal renal


angioplasty
PO2

partial oxygen pressure

PSV peak systolic velocity


RAS renal artery stenosis
RAR
8

renoaortic ratio

RI

resistive index

T99m technetium 99 metastable


WHO world health organization

List of Tables
Tabl
e
2-1

Name

Page
No

Causes of increased RI in renal arteries


9

24

2-2

Different sonographic criteria used for


diagnosing renal
artery stenosis

24

4-1
4-2
4-3

Frequency of Renal Artery Stenosis


Frequency distribution of patients according to age
Frequency distribution of patients according to gender

32
33
34

4-4
4-5

Frequency distribution of patients according to occupation


Frequency distribution of patients according to HTN

35
36

4-6

duration
Frequency

37

4-7
4-8
4-9

comorbidities
Frequency distribution of patients according to RFTs
statistics of doppler values and kidney lengths
Frequency distribution of patients according to spectral

38
49
44

4-10

waveform
Frequency distribution of patients according to other

45

4-11
4-12
4-13
4-14
4-15
4-16
4-17
4-18
4-19
4-20

distribution

of

patients

according

to

sonographic abnormalities
age * Renal artery stenosis Cross tabulation
gender * Renal artery stenosis Crosstabulation
HTN duration * Renal artery stenosis
Crosstabulation
co mrbidities * Renal artery stenosis
Crosstabulation
RFTs * Renal artery stenosis Crosstabulation
other sonographic abnormalities * Renal artery
stenosis Crosstabulation
HTN duration* Rt renal artery RI
Crosstabulation
HTN duration*Lt renal artery RI
Crosstabulation
RFTs*Rt renal artery RI Crosstabulation
RFTs *Lt renal artery RI Crosstabulation

10

46
47
48
49
50
51
52
53
54
55

List of Figures
Figur

Name

Page No

e
2-1
2-2

Normal vascular anatomy of the kidney


6
CTA MIP image, displaying normal Right and Left 12

2-3
2-4
4-1
4-2
4-3
4-4
4-5
4-6

Renal arteries
DSA showing RAS due to fibromuscular dysplasia
Renal artery stenosis
Frequency of Renal Artery Stenosis
Frequency distribution of patients according to age
Frequency distribution of patients according to gender
Frequency distribution of patients according to occupation
Frequency distribution of patients according to HTN duration
Frequency distribution of patients according to comorbidities

4-7
4-8
4-9
4-10
4-11
4-12
4-13
4-14
4-15
4-16
4-17
4-18
4-19
4-20
4-21
4-22

Frequency distribution of patients according to RFTs


Frequency distribution of patients according to Rt kidney length
Frequency distribution of patients according to Lt kidney length
Frequency distribution of patients according to Rt kidney PSV
Frequency distribution of patients according to Lt kidney PSV
Frequency distribution of patients according to Rt kidney RI
Frequency distribution of patients according to Lt kidney RI
Frequency distribution of patients according to Rt kidney R/A
ratio
Frequency distribution of patients according toLt kidney R/A
ratio
Frequency distribution of patients according to spectral
waveform
Frequency distribution of patients according to other sonographic
abnormalities
age * Renal artery stenosis Cross tabulation
gender * Renal artery stenosis Crosstabulation
HTN duration * Renal artery stenosis
Crosstabulation
co mrbidities * Renal artery stenosis Crosstabulation
RFTs * Renal artery stenosis Crosstabulation
11

16
21
32
33
34
35
36
37
38
40
40
41
41
42
42
43
43
44
45
46
47
48
49
50

4-23
4-24
4-25
4-26
4-27

other sonographic abnormalities * Renal artery


stenosis Crosstabulation
HTN duration* Rt renal artery RI Crosstabulation
HTN duration*Lt renal artery RI Crosstabulation
RFTs*Rt renal artery RI Crosstabulation
RFTs*Lt renal artery RI Crosstabulation

12

51
52
53
54
55

Chapter One
Introduction

Chapter One
1.1. Introduction
1.1.1. definitions

13

High blood pressure (hypertension) is a major factor in the


pathogenesis of coronary heart disease, stroke and renal failure .
The World Health Organization has defined hypertension as a
systolic blood pressure of 140 mmHg or greater and/or a diastolic
blood pressure of 90 mmHg or greater in subjects who are not
receiving antihypertensive medication. Hypertension is further
stratified

into

two

categories,

essential

and

secondary

hypertension. Known secondary forms of hypertension account for


approximately 10% of all cases of hypertension. Secondary forms
are often considered in patients who have clinical features that
are inconsistent with essential hypertension. Common general
clinical clues are an unusual age at onset (younger or older than
for essential hypertension), a sudden, unexplained increase in
blood pressure from a previous state of control, or primary or
acquired resistance to treatment. Secondary causes include
drugs, increasing obesity, and obstructive sleep apnea. The
clinical clues suggestive of secondary hypertension should be
recognized, and when secondary hypertension is suspected,
consultation with a subspecialist should be considered. (1)
Renovascular hypertension is the most common form of
potentially curable secondary hypertension. It occurs in 1% to 3%
of the general hypertensive population, in 10% of persons with
resistant

hypertension,

and

in

up to

30%

of those

with

hypertensive crisis. It is less common in African Americans than in


Caucasians.(1)

14

Renal artery stenosis is commonly caused by either


fibromuscular

dysplasia

or

atherosclerosis.

Atherosclerotic

stenosis virtually always occur at the origins of the renal arteries


from the aorta or, very rarely, at the branching into segmental
arteries. They predominantly affect older males with other
obstructive vascular diseases. In contrast fibromuscular stenosis
nearly exclusively involves the middle thirds of the renal arteries
and primarily occurs in young women. Hence, selective duplex
scanning of the respective renal artery segment according to the
suspected cause of stenosis can be performed. (2)

1.1.2. Screening Tests


Although several tests are available to screen for renal
artery

stenosis,

duplex

renal

ultrasonography,

magnetic

resonance angiography, and spiral computed tomographic (CT)


angiography are considered the initial screening tests of choice. (1)
Duplex ultrasonography is noninvasive and does not use
contrast media. Its usefulness extends to persons who have renal
insufficiency or a history of contrast allergy. Performance of the
test does not require discontinuation of any antihypertensive
drug. It is of low cost, widely available, relatively easy to perform,
requires minimal patient preparation, and does not use ionizing
radiation . It identifies increases in blood flow velocity that occur
with luminal narrowing of a renal artery.

(1)

Criteria for a positive test are 1) a ratio of peak flow velocity in


the involved renal artery to peak flow velocity in the aortaof more
15

than 3.5 and 2) renal artery peak systolic flow of 180 cm/s or
more.(1)

1.1.3. importance of the study


According to world health statistic published by WHO in
2013, the prevalence of raised blood pressure in Sudan in 2011
was 40% .
1985

(3)

This represents a considerable rise from 7.5% in

through 18.2%

in

2002.

(4)

A study

about renal

replacement therapy in Sudan revealed that hypertension was


the most commonly reported cause of ESRD (26.1%).The
diagnosis

of

hypertensive

nephrosclerosis

is

difficult

to

ascertain even in patients with long standing hypertension.


Such patients may have had secondary hypertension due to
undiagnosed kidney disease.(5)
Early literature indicated the potential of doppler for
improving the sonographic assessment of renal dysfunction.
Changes in intrarenal spectra (quantified using RI) were
associated with acute or chronic urinary obstruction, several
intrinsic native renal diseases, renal transplant rejection, and
renal vascular disease. . A review indicated that most
physicians do not refer these patients for doppler study, which
may have been caused by a lack of understanding of the
hemodynamic changes that influence doppler spectra .(6)

16

1.2.Objectives
1.2.1. General Objective
To estimate the frequency of renal artery stenosis among
hypertensive patients in Khartoum using duplex sonography .

1.2.2. Specific Objectives


1. To evaluate the relation between renal artery stenosis and
age, gender, and other co morbidities of the patient
2. . To explore other kidney sonographic abnormalities that may
associate renal artery stenosis.
3. To evaluate the relation of measurable doppler values with
the duration of hypertension, and renal function in
hypertensive patients.

17

Chapter Two
Literature Review & Background
Studies

18

Chapter Two
2. Literature Review
2.1.Historical Background
As early as in 1836, Richard Bright reported the first potential
association between hypertension and renal disease when he
associated autopsy findings of kidney disease and cardiac
hypertrophy to an increased peripheral resistance .

(7)

In 1898 Tigerstedt and Bergman discovered that extract from the


renal cortex of rabbits caused a marked increase in arterial
pressure when injected intravenously (i.v.) to normotensive
rabbits(8). They hypothesized that the renal cortical tissue extract
contained a hypertensive factor and hence named it renin
19

(8)

The first successful experimental model of arterial hypertension


caused by manipulation of the kidney was developed in 1934
when Goldblatt et al. showed that clamping of renal arteries in
dogs produced a reproducible and persistent rise in AP. (9)
Clamping other large arteries as splenic or femoral arteries had
no effect on AP, indicating that hypertension resulted specifically
from renal ischemia caused by renal artery stenosis (RAS) 4. In
1938, Leadbetter and Burkland reported the first successful
treatment of hypertension by nephrectomy in a patient with RAS.
Treatment of RAS changed with the introduction of surgical
revascularization in 1954 6 and later on, in 1978, with the
introduction of percutaneous transluminal renal angioplasty
(PTRA)(9).

Figure 2.1 : Normal vascular anatomy of the kidney(9)

2.2.Renal Circulation Anatomy and Physiology

20

The kidneys play an essential role in maintaining a stable


internal milieu for optimal cellular function (homeostasis) through
the excretion of metabolic waste products and adjustment of
urinary excretion of water and electrolytes. To achieve this
homeostatic function, a high proportion of cardiac output (2025%) passes through the renal circulation producing about 180
liters of glomerular filtrate (primary urine) per day. In the tubular
system the reabsorption of water and electrolytes is adjusted to
match the prevailing needs while waste products are retained in
the urine and excreted. Almost all ( 99%) of the filtered water
and sodium is normally reabsorbed in the tubules . (10,11)
The kidneys receive their blood supply from the main renal
arteries which arise from the abdominal aorta. Before reaching
the hilum of the kidney, the renal artery generally divides into
anterior and posterior branches which in turn give rise to four or
five segmental arteries. The segmental arteries divide into
interlobar arteries, which progress towards the cortex. At the
junction between the cortex and medulla, interlobar arteries
change course and become arcuate arteries that run in parallel to
the kidney surface. These, in turn, give rise to interlobular arteries
which radiate into the cortex and divide into afferent arterioles
supplying blood to the glomeruli. Each afferent arteriole supplies
blood to a glomerulus, a tuft of capillaries attached to the
mesangium and enclosed in Bowmans capsule. Glomeruli are
drained by efferent arterioles that in the cortex give rise to the
peritubular

capillary

plexus

.
21

Efferent

arterioles

from

juxtamedullary glomeruli form vasa recta capillaries that form


long hair-pin loops that turn in the medulla

. Thus, the renal

circulation consists of two capillary beds connected in series by


the efferent arteriole. The first in the series is the glomerular
capillary bed which is the site of filtration and formation of
primary urine and the second is the peritubular capillary bed
which transports reabsorbed water and solutes back to the
systemic circulation. Total renal blood flow (RBF) in a healthy adult
is approximately 1.2 L/min which corresponds to about 20-25% of
cardiac output. The high RBF is required to maintain a high GFR
and effective excretion of waste products. Consequently, oxygen
delivery to the kidneys is very high and renal oxygen extraction
low. However, there is a marked regional difference in blood flow
distribution in the kidney . About 90% of total RBF is distributed to
the cortex where the partial pressure of oxygen (pO2) is high (
50 mmHg), whereas approximately 10% of RBF goes to the
medulla where the pO2 is low ( 10-20 mmHg). In addition,
oxygen consumption in the outer medulla (OM) is high due to
active transport of sodium in the thick ascending loop of Henle
making the OM vulnerable to ischemic injury . However, low local
blood flow in the medulla also plays important physiological roles
in preventing washout of the medullary hyperosmotic gradient
which is necessary for effective water reabsorption and urine
concentration.

(10,11)

2.3.Etiology of renal artery stenosis

22

RAS can be caused by a variety of lesions. In Western


populations atherosclerosis and fibromuscular dysplasia (FMD) are
the main two causes of RAS. Atherosclerosis accounts for about
90% of all cases of RAS. These lesions are commonly ostial and
are in many cases extensions of atheromatous aortic plaques that
involve the proximal 1-2 cm of the renal artery 23, 24. Patients
with ARAS are typically over the age of 50 years and males are
more commonly affected than females. ARAS is usually a
manifestation of generalized atherosclerosis and hence these
patients frequently have coronary artery disease (about 20 %)
and peripheral vascular disease (about 35 %) 23, 24. FMD
accounts for about 10% of all cases of RAS. Medial fibroplasia is
the most common subtype of FMD (7580%) . The right renal
artery is more commonly affected and the disease is most
prevalent in 25- to 50- year old females .

(12,13)

FMD may involve other major arteries, commonly internal


carotid arteries, and less often the vertebral, iliac, subclavian,
visceral and coronary arteries. The etiology of FMD is unknown
although a number of factors have been suggested, including:
a) genetic predisposition.
b) hormonal influence, in view of the predominance in females.
c) mechanical factors, such as stretching and trauma to the blood
vessel wall, and d) ischemia of the vascular wall due to fibrotic
occlusion of the vasa vasorum,(1)

23

2.4. Pathophysiology of Renovascular Hypertension


Critical stenosis of a renal artery (i.e., 70% luminal
narrowing) increases renin production from the ischemic kidney.
Renin acts on circulating renin substrate to produce angiotensin I,
which is converted to angiotensin II (a potent vasoconstrictor) by
ACE in the lung and other tissues. In addition to vasoconstriction,
angiotensin II directly increases renal sodium reabsorption and
also stimulates aldosterone production, resulting in extracellular
volume expansion. Angiotensin II also stimulates the sympathetic
nervous system, contributing further to increased vascular
resistance, and stimulates thirst and the release of vasopressin,
contributing

further

to

increased

extracellular

volume.

In

unilateral disease, the nonischemic kidney is subjected to


increased perfusion, resulting in higher sodium excretion and
suppression of renin release. These effects lessen the degree of
hypertension but perpetuate underperfusion of the ischemic
kidney, which, in turn, perpetuates excess renin production. In
bilateral disease, initial increases in renin cause extracellular
volume expansion and volume-dependent hypertension, which
persists because there is no contralateral normal kidney to
excrete more sodium. In persons with bilateral disease, the
hypertension is volume dependent but becomes renin dependent
with extracellular volume depletion. Correcting renal ischemia
24

eliminates the stimulus for excess rennin release and can cure or
lessen hypertension. In unilateral renal artery stenosis, prolonged
hypertension

eventually

causes

nephrosclerosis

in

the

nonischemic kidney (in combination with other cardiovascular risk


factors) or ischemic injury to the involved kidney. If either occurs,
relieving renal arterial stenosis may not cure hypertension. The
longer the duration of hypertension before diagnosis, the greater
the likelihood of these untoward renal outcomes and the less the
likelihood of cure of hypertension with intervention. (1)

2.5.Clinical Clues of Renovascular Hypertension


Clues suggesting renovascular hypertension include lack of a
family history of hypertension, onset of hypertension before age
30 (consider fibromuscular dysplasia, especially in a woman),
onset of hypertension after age 50 (consider atherosclerotic
renovascular disease, especially in a smoker or a person with
coronary

or

peripheral

arterial

disease),

presentation

with

accelerated or malignant hypertension, or sudden worsening of


preexisting hypertension in a middle-aged or older person
(renovascular

hypertension

superimposed

on

essential

hypertension). Persons with cardiovascular risk factors (tobacco


use, hyperlipidemia, or diabetes) are at increased risk of
atherosclerotic renal artery stenosis. The most important physical
finding is an abdominal bruit, especially a high-pitched systolicdiastolic bruit in the upper abdomen or flank. However, 50% of
persons with renovascular hypertension do not have this finding.
25

Other physical clues are severe retinopathy of accelerated or


malignant

hypertension

(hemorrhages,

exudates,

and

papilledema) or evidence of atherosclerotic occlusive disease in


other vascular beds (atherosclerotic renal artery stenosis of >50%
is observed in up to 20% of persons with coronary artery disease
and in up to 50% of persons with peripheral arterial disease).
Laboratory abnormalities are hypokalemia (due to secondary
aldosteronism), an increased serum level of creatinine, proteinuria
(rarely in the nephrotic range), and a small kidney seen on an
imaging study. Underlying bilateral renal artery stenosis may be
indicated by an acute decline in renal function (20% increase in
serum creatinine) either after the initiation of therapy with an
ACEI or an ARB or after a drug-induced, sudden decrease in blood
pressure. Other signs in patients presenting with bilateral renal
artery stenosis (i.e., ischemic nephropathy) include the sudden
development of pulmonary edema accompanied by severe
hypertension (flash pulmonary edema), frequent episodes of
symptomatic congestive heart failure accompanied by increases
in blood pressure, or a subacute decline in renal function with or
without worsening hypertension. Patients with atheroembolic
renal disease may also present with a sudden onset or worsening
of hypertension and a subacute decline in renal function.
Historical clues (e.g., occurrence after angiography or vascular
surgery), physical findings (distal livedo reticularis and peripheral
emboli), and laboratory abnormalities (increased erythrocyte
sedimentation

rate,

anemia,

hematuria,
26

eosinophilia,

and

eosinophiluria) help identify this disorder. In young persons who


have hypertension (even if not severe) of short duration and
suggestive clinical features, evaluation for renovascular disease is
indicated. Renal artery stenosis in these persons can be identified
and corrected with a low risk of morbidity and mortality and a
high probability of cure. Older persons should be evaluated for
renovascular hypertension on a selective basis. In general,
selection should be restricted to persons who have suggestive
clinical features and blood pressure that cannot be controlled
medically or who have an unexplained, observed decline in renal
function or a cardiorenal syndrome (recurrent flash pulmonary
edema or resistant heart failure) and who are considered
reasonable risks for (and are willing to undergo) interventional
therapy.(1)

2.6.Screening Tests
Duplex Ultrasonography will be discussed later.
2.6.1.Magnetic Resonance Angiography
Magnetic resonance angiography (MRA) visualizes the main
renal arteries without use of a radiocontrast agent or exposure to
radiation.

Its

usefulness

extends

to

persons

with

renal

insufficiency or those with a history of radiocontrast allergy. Also,


it is a reasonable choice for persons with a high likelihood of the
disorder who have concomitant severe, diffuse atherosclerosis
and, thus, are at high risk of atheroembolization with angiography.
Field limitations may decrease the ability to see lesions in the
27

distal main renal arteries or lesions in branch vessels (common


sites of fibromuscular disease). Accessory renal arteries may not
be

identified,

the

degree

of

arterial

stenosis

may

be

overestimated, and persons prone to claustrophobia may not


tolerate being placed in the magnetic resonance equipment.
Renal stents cause imaging artifacts, and persons with cardiac
pacemakers, metallic artificial cardiac valves, or cerebral artery
aneurysm clips cannot be imaged. Sensitivity is 80% to 90% (less
for fibromuscular dysplasia), and specificity is 90%. This is an
expensive screening test.1

Fig 2.2: CTA MIP image, displaying normal Right and Left Renal
arteries.(2)

28

2.6.2.Spiral Computed Tomographic Angiography


Spiral CT angiography offers excellent three-dimensional
images but requires a considerable amount of radiocontrast agent
and patient cooperation. This is an option for persons with normal
renal function who do not have a contrast allergy and in whom
MRA is contraindicated. Renal stents do not cause imaging
artifacts. Sensitivity and specificity are similar to those for MRA.
This is also an expensive test. Other noninvasive tests are
available to screen for renal artery stenosis; however, they are
used less often because the test characteristics are inferior
compared with those of duplex ultrasonography, MRA, and spiral
CT angiography.(1)
Historically, the intravenous pyelogram (IVP) was the
mainstay screening test for renovascular hypertension. For
screening, radiographs that are taken at 1-minute intervals for the
first 5 minutes after injection of contrast medium are used to
identify a delay in the appearance of contrast medium in the renal
collecting system on the side of a renal artery stenosis. This is
referred to as the hypertensive IVP. Characteristic findings on a
hypertensive IVP suggesting renal artery stenosis are:
1) unilateral reduction in renal size (1.5-cm decrease in pole-topole diameter of the smaller kidney);
2) delayed appearance of contrast medium in the collecting
system of the ischemic kidney;

29

3) hyperconcentration of contrast medium in the ischemic


kidney;
4) ureteral scalloping by collateral vessels; and
5) cortical thinning or irregularity. Sensitivity is 70% to 75%, and
specificity is 85%.(1)
2.6.3.Captopril Radionuclide Renal Scan
Some still consider the captopril radionuclide renal scan to be
a useful screening test. However, recent reviews suggest a lower
test sensitivity than was reported earlier. Currently, sensitivity is
estimated at 75% and specificity at 85%. Pretest treatment of
patients with captopril (25-50 mg given 1 hour before isotope
injection) increases the sensitivity of the scan compared with that
of standard renography. The rationale is that glomerular filtration
in an ischemic kidney depends on the vasoconstricting effect of
angiotensin II on the efferent arteriole of the nephron to maintain
effective transglomerular filtration pressure. Treatment with an
ACEI causes efferent arteriolar dilatation, with loss of filtration
pressure in the nephron. This causes a decline of glomerular
filtration in the ischemic kidney, with less of an effect on renal
blood flow. These changes are identified with the scanning
technique. The radionuclides used most commonly are iodine 131
orthoiodohippuric acid (OIH) and Tc-99m mercaptoacetyltriglycine
(MAG3), which are markers for renal blood flow (they are excreted
primarily

by

renal

tubular

secretion),

and

Tc-99m

diethylenetriamine pentaacetic acid (DPTA), which is a marker for


30

glomerular filtration rate (it is excreted primarily by glomerular


filtration). Criteria for a positive test with DPTA are time to peak
activity in the kidney of 11 minutes or more and a ratio of the
glomerular filtration rate between the kidneys of 1.5 or more. The
criterion for a positive test with OIH or MAG3 is residual cortical
activity at 20 minutes of 30% or more of peak activity. The renal
scan is safe for persons with a history of contrast allergy. The
interpretive value is reduced by renal insufficiency (creatinine
>2.0 mg/dL) or by bilateral or branch renal artery disease. Urinary
outflow obstruction may mimic renal artery stenosis. .(1)
2.6.4.Captopril Test
Acute blockade of angiotensin II formation by ACEIs induces a
reactive increase in PRA. The magnitude of this increase is usually
greater

in

renovascular

hypertension

than

in

essential

hypertension and is the basis for the captopril test. The use of
antihypertensive drugs that influence the renin-angiotensinaldosterone axis must be discontinued for several days before the
test. PRA is measured at baseline and at 60 minutes after
administering captopril orally. Criteria for a positive test are 1)
PRA of more than 12 ng/mL per hour after administration of
captopril, 2) absolute increase in PRA over baseline of at least 10
ng/mL per hour, and 3) increase in PRA of 150% or more if the
baseline PRA is more than 3 ng/mL per hour or 400% or more if
the baseline PRA is less than 3 ng/mL per hour. The results are
compromised if the person has renal insufficiency. Sensitivity is
39% to 100%, and specificity is 72% to 100%. Because the results
31

can be influenced by many factors that are difficult to identify and


control, predictive accuracy is low. .(1)
2.6.5.Renal Vein Renins
Lateralization of renal vein renins is a good predictor of a
favorable outcome after intervention for unilateral renal artery
stenosis; however, because many factors that influence renin
secretion are difficult to identify and control (as noted for the
captopril test), the predictive value of the test is low. It is invasive
and expensive. Lateralization is present if the ratio of renin
activity on the affected side compared with that on the normal
side is 1.5:1.0 or more. Sensitivity is 63% to 77%, and specificity
is 60% to 95%.(1)
2.6.6.Digital Venous Subtraction Angiography
Digital venous subtraction angiography uses contrast media,
but access to the circulation is through a peripheral vein. With the
advent of newer screening tests, it is used less often. This
technique provides adequate visualization of the proximal portion
of the main renal arteries (usual location of atherosclerotic
disease) in 90% of persons but less effective visualization of the
distal portions of the main renal arteries or branches (the usual
location of fibromuscular dysplasia). This technique is expensive,
and in 20% to 30% of persons, neither renal artery is identified
because of superimposition of abdominal vessels or patient
motion. Both the sensitivity and the specificity are 85% to 90%. (1)

32

Figure 2.3 : DSA showing RAS due to fibromuscular dysplasia. (6)

2.6.7.Renal Arteriography
Conventional renal arteriography is the diagnostic standard
test to identify renal artery stenosis. In clinical situations in which
the pretest likelihood is high (50%), a negative result from a
screening test still leaves a significant posttest probability of
disease (20%). Thus, in these settings, consideration should be
given to performing renal angiography without first performing
screening tests. Exceptions maybe when patients have diabetes
or severe generalized atherosclerosis with concomitant renal
insufficiency and use of a noninvasive test initially, such as MRA
or duplex ultrasonography, may be reasonable. This is because in
33

these settings, the risk of contrastinduced acute renal failure or


atheroembolism is significant. Contrast toxicity from angiography
can be reduced with the use of gadolinium or carbon dioxide as
the contrast agent. However, these techniques do not reduce the
risk of atheroembolism..(1)

2.7.Therapy for Renovascular Hypertension


Options for the management of renovascular hypertension
include

medical

and

interventional

therapies.

Percutaneous

balloon angioplasty, stent placement, and surgical procedures to


relieve renal ischemia are the interventional treatments. Goals of
interventional therapy are to cure or improve hypertension or to
preserve renal function. Medical therapy is reserved for persons
who are not considered candidates for interventional therapy
(because of the extent or location of the vascular lesions, high
surgical risk, or uncertainty about the causative significance of
the lesion) or who are unwilling to undergo interventional therapy.
As noted earlier, selection of persons for screening excludes older
persons

with

controlled

hypertension

and

no

evidence

of

progressive renal dysfunction even if renovascular disease is


suspected.

Percutaneous

transluminal

angioplasty

is

the

treatment of choice for amenable lesions caused by fibromuscular


dysplasia and is an option with or without stent placement in
some cases of atherosclerotic renovascular disease. Hypertension
is cured in 50% and improved in 35%

of persons with

fibromuscular dysplasia. The failure rate is 15%. In contrast,


34

hypertension is cured in 20% and improved in 50%, with a failure


rate of 30%, in persons with atherosclerotic renovascular disease.
Complications of angioplasty include groin hematoma, dyeinduced azotemia, dissection of the renal artery, renal infarction,
and, rarely, rupture of the renal artery, with the potential for loss
of

the

kidney

and

the

need

for

immediate

surgery.

Atheroembolization is a risk in older persons with diffuse


atherosclerosis . Stent-supported angioplasty is an appropriate
option for some persons with atherosclerotic renal artery stenosis,
especially for orificial disease. In the presence of aneurysmal or
severe atherosclerotic disease
of the aorta requiring concomitant aortic reconstruction, or in
persons in whom percutaneous intervention has failed, surgical
intervention is the treatment of choice. Kidneys with a pole-topole

length

of

cm

or

less

should

be

removednot

revascularizedif intervention is indicated and removal will not


jeopardize overall renal function. The role of interventional
therapy for preservation of renal function in ischemic nephropathy
is

uncertain.

In

most

cases,

the

underlying

disease

is

atherosclerosis. Improvement in renal function, defined as a


decrease in serum creatinine, occurs in 30% of cases. In
approximately 50% of cases, the creatinine level does not
decrease; however, benefit may be defined as stabilization of
renal function. Of concern is that in 20% of cases, renal function
deteriorates rapidly after the intervention, most likely from a
combination of several factors, including contrast toxicity, acute
35

renal artery thrombosis, or atheroembolization. The medical


treatment of renovascular hypertension is not different from that
of

essential

hypertension.

Both

volume

retention

(due

to

aldosterone) and vasoconstriction (due to activation of the


sympathetic nervous system and angiotensin II) contribute to the
elevation of blood pressure. ACEIs and ARBs can precipitate acute
renal failure in the presence of bilateral renal artery stenosis.
Medical treatment does not correct the underlying ischemia of the
affected kidney, and decreases in systemic blood pressure may
further

aggravate

loss

of

renal

function.

Progression

of

atherosclerotic renal artery disease can be slowed by control of all


modifiable risk factors, including the use of statin drugs for
aggressive lowering of cholesterol. In medically managed persons,
renal function should be followed carefully because deterioration
may be a sign of progressive disease . (1)

2.8.Duplex Ultrasound of the Renal Artery


Duplex ultrasonography is noninvasive and does not use
contrast media. Its usefulness extends to persons who have renal
insufficiency or a history of contrast allergy. Performance of the
test does not require discontinuation of any antihypertensive
drug. therapy, and it provides information on kidney size, screens
for obstructive uropathy and aortic aneurysm, and identifies
bilateralrenal artery

stenosis. Overlying bowel gas or other

technical problems limit the complete study of both renal arteries

36

in up to 50% of cases. Often, accessory or branch vessel disease


is not identified. The sensitivity and specificity are 75% to 80%. (1)

2.8.1.Examination Technique
One way of identifying the renal arteries at their origins just
below the easily visualized superior mesenteric artery is to
localize the latter in transverse orientation and to then move the
transducer 12 cm downward and look for the renal arteries as
they arise from the aorta to the left and right . A second landmark
is

the

left

renal

vein

(hypoechoic,

broader

band)

which

overcrosses the aorta before


opening into the vena cava and along its route passes between
the superior mesenteric artery and the aorta. The left renal artery
typically arises some millimeters below the right renal artery and
both do not usually take a strictly horizontalcourse but move
slightly downward. The right renal artery first courses anteriorly in
a slightly curved fashion and then arches underneath the vena
cava. The origins as well as the first 3 cm of the renal arteries can
be visualized and evaluated in over 90% of cases while
visualization of the middle third is often incomplete due to
overlying bowel gas, especially on the left. The middle segment of
the renal artery is easier to scan on the right where the vena cava
can serve as an acoustic window. Interfering bowel gas can be
displaced by pressing the transducer against the bowel until the
vessel is seen. The transducer is then moved to the right or left to
achieve an optimal angle for sampling of the Doppler spectrum.
37

The distal third can be scanned continuously from the flank


starting at the renal hilum and following the course of the vessel
proximally . From this transducer position, it is also possible to
continuously record an adequate Doppler spectrum with a
relatively small angle. The individual segmental arteries are
identified in the color flow mode and evaluated for stenoses at
their origins during shallow breathing or breath-holding. If renal
artery infarction is suspected, the renal parenchyma is evaluated
for perfusion defects that are seen on color duplex scans as
wedge-shaped areas without color coding (high but artifact-free
gain, low pulse repetition frequency).(2)

2.8.2.Normal Findings
Supplying a low-resistance parenchymal organ, the renal
arteries have a flow profile with little pulsatility and a large
diastolic component. Measurements performed in 102 renal
arteries without abnormalities on control angiography yielded a
mean peak systolic velocity of 84.7 13.9 cm/s and an enddiastolic velocity of 31.2 7.8 cm/s. The Pourcelot index was 0.66
0.07 (findings by our group, 1988). Visualization of the renal
arteries for exclusion of a stenosis by duplex scanning is possible
in 8590% of cases; the proximal third as the preferred site of
atherosclerotic stenoses can be evaluated in over 90%of cases.
The flow velocities reported in the literature vary widely from one
study to the next but also within the studies. The range is 60140
cm/s for peak systolic velocity and 2065 cm/s for end-diastolic
38

velocity with a Pourcelot index of 0.60.8. Reported diameters


range from 58 mmThe peak systolic and diastolic velocities and
the Pourcelot index are affected by vessel elasticity and
peripheral resistance. Moreover, they are influenced by systemic
blood pressure. In diabetics, medial sclerosis with decreased wall
elasticity and parenchymal changes result in a decreased diastolic
flow and a higher Pourcelot index. Peak systolic velocity is slightly
higher than in subjects with normal vessels.

(2)

Figure 2.4 : Renal artery stenosis. A, Intrarenal spectral


waveform shows a tardus-parvus signal with a prolonged
acceleration time and low resistive index (RI). B, Waveform at the
origin of the renal artery from the aorta shows a high peak
velocity of 410 cm/sec with an RI of 0.43.(6)

2.8.3.Doppler Interpretation
There are many proposed guidelines for Doppler interpretation.
Proposed parameters to assess for stenosis include the peak
39

systolic velocity (PSV), renal aortic ratio (RAR; defined as highest


systolic velocity in renal artery divided by aortic systolic velocity,
with

aortic

velocity

measured

at

or

above

SMA

origin),

acceleration time, acceleration index, renal interlobar ratio, and


renal-renal ratio. The Cleveland Clinic used a combination of RAR
of 3.5 or greater or PSV of 200 or greater as the criterion for renal
artery stenosis of more than 60%. We use a variation of the
Cleveland Clinic guidelines, using the same RAR as the study but
a higher PSV. We have done internal validation of our guidelines
but

continue

to

look

for

ways

to

improve

them.

False-

Positive/False-Negative Results. To obtain the highest accuracy, it


is important to avoid relying solely on the numerical data
obtained. When a high velocity is seen or when the renal aortic
ratio is high, the interpreting radiologist must also actively look
for secondary signs of stenosis, such as a characteristic harsh
audible signal at the site of stenosis, increased diastolic flow,
color

bruit,

and

post-stenotic turbulence.

Without

ancillary

findings, the interpreter must consider the possibility that the


high velocity or high RAR represents a false-positive result. Falsenegative findings are most a risk when visualization is marginal
and the entire artery has not been adequately evaluated. In
perhaps 5% to 10% of patients, accurate diagnosis cannot be
made because of inadequate visualization of one or both arteries.
Attention to intrarenal waveforms is also of some importance. A
highly abnormal waveform can be a valuable indicator of stenosis.
A delayed systolic peak (tardus, i.e., tardy) and velocities that
40

are greatly decreased (parvus, i.e., puny) can be a strong sign


of a more proximal stenosis. The intrarenal waveform can be
analyzed quantitatively by calculating the systolic rise time and
the acceleration . Although we calculate these parameters, a
qualitative assessment of the appearance of the waveform
usually serves just as well. We only rely on a tardus-parvus
waveform to make the diagnosis when the finding is pronounced.
An acceleration time greater than 0.07 second and a slope of
systolic upstroke less than 3 m/s2 are suggested as thresholds to
assess for renal artery stenosis. Simple recognition of the change
in pattern may be adequate. Pharmacologic manipulation with
captopril may enhance the waveform abnormalities in patients
with renal artery stenosis. Doppler sonography remains a
controversial technique for the detection of native renal artery
stenosis. The use of intravascular contrast agents increases the
technical success rate for the evaluation of renal artery stenosis.
It may also play a role in the assessment and follow-up of patients
undergoing renal artery angioplasty and stent placement .(6)
The examination is challenging to the uninitiated operator, but
establishment of a renal artery duplex Doppler program can be
rewarding. Because of the lower cost versus other diagnostic
tests, Doppler ultrasound lowers the threshold for the diagnosis of
renovascular hypertension. Hurdles mainly relate to the learning
curve and the initial investment of time. Starting a program is
more feasible in a large center where demand will likely be higher

41

than in a smaller facility. Once the program is mature, the study is


financially viable and can result in improved patient care

table (2.1): Causes of increased RI in renal arteries.

.(6)

(6)

Table( 2.2) : Different sonographic criteria used for diagnosing


renal artery stenosis.(2)

42

2.9. Background Comparative Studies


The average incidence of renovascular hypertension is 1 to
4%in an unselected population (von Bockel et al. 1989; Foster et
al. 1973; Olbricht et al. 1991) but incidences as low as 0.18% and
as high as 20% have also been reported (Arlart and Ingrisch 1984;
Tucker and Lebbarthe 1977). These discrepancies are due to the
use of different screening methods and the investigation of
different groups of the normal population and patients (presence
of vascular risk factors and accompanying diseases, selected
patient groups).(2)
Hansen et al, used ultrasonography to screen 870 people over
age 65 and found a lesion (a narrowing of more than 60%) in
6.8%.(2)
43

A population based study in Denemark about the prevalence of


renal artery stenosis in subjects with moderate to severe
hypertension by Andersen UB , Borglykke A, and
examined

332

subjects

aged

50-66

years

Jorgensen T,

using

doppler

ultrasound, with blood pressure <160\100, found the prevalence


to be 3.3% in the examined population. (19)
Benjamin MM, Fezal P, Filardo G, and Stoler RC, studied the
prevalence and risk factors of renal artery stenosis in patients
with resistant hypertension, they examined 285 patients , the
mean age was 72.5 years, 24.2% of

them had

renal artery

stenosis on angiography.(18)
Jonathan Valabhji, Stephen Robinson, Claire Poulter, Adam C.J.
Robinson, Chantal Kong, Christoph Henzen, and others, studied
the prevalence of Renal Artery Stenosis in Subjects With Type 2
Diabetes and Coexistent Hypertension, A total of 117 subjects
with type 2 diabetes and coexistent hypertension between 40 and
70 years of age, The prevalence of RAS detected by using MRA in
117 hypertensive type 2 diabetic subjects was 17%. (17)
Akram A. Saleh, , Basem B. Bustami, studied the Prevalence of
renal artery stenosis in patients undergoing routine cardiac
catheterization , Of the 354 patients, 285 had coronary artery
disease and 27 had RAS. Significant RAS was present in 11
patients.(16)
Ala Mohammed Abd Elgyoum Mohamed Ahmed1, Abd Allah
Mohammed Jaber, and Amin A. E. Elzaki studied
44

doppler

ultrasonography of the kidneys in diabetic patients in Khartoum in


2013 and found that the examination of Doppler for 47patient
showed that 93.6% of patients had ordinary renal artery
resistance and 6.4% had high resistance. The study also showed
that there were relations between the affection period of diabetic
mellitus & changes happening in the kidneys such as renal failure
29.8%, pyelonephritis is 2.1%, renal artery stenosis 6.4%. there
was association between renal artery resistance index and
pulsatility index with diabetic patients who had renal failure and
renal artery stenosis.(15)
Ohta, Yuko; Fujii, Koji; Arima, Hisatomi; Matsumura, Kiyoshi;
Tsuchihashi, Takuya; Tokumoto, and
found increased

Masanori in Japan

2005,

renal resistive index in atherosclerosis and

diabetic nephropathy assessed by Doppler sonography. (14)

45

Chapter Three
Materials and Methods

46

Chapter Three
3. Methods and Materials
3.1. Study Design
This is a retrospective cross-sectional study descriptive study.

3.2. Study Area


Ultrasound departments in Khartoum city hospitals , namely in
Soba University Hospital, Sharq El-Niel, Khartoum North, and
Umdorman Military Hospital .

3.3. Study Population and Sample


Sample was drawn randomly from hypertensive patients
referred to ultrasound departments at hospitals under study .
Total number of 100 patient was examined with doppler
ultrasonography.

3.4. Technique and Equipments


Gray scale examination, color and spectral Doppler
sonographic studies was performed with the ultrasound machines
available at study centers, which are Toshiba Nemio 20 (Toshiba,
Japan), Siemens sonoline G60S (Siemens, USA), Mindray DC-N3
(Mindray, Germany), and Landwind Mirror2 (Landwind China).
Either a 3.5- or 5.0-MHz curvilinear array transducers

with

variable focal zone were used. Patients were prepared as usual by


taking nothing by mouth but clear fluids 8 hours preceding the
47

examination. Patients were examined in supine, left or right


lateral, or prone positions if needed as stated by the protocols.
The coupling gel was generously applied. Each Kidney was
examined with gray scale in at least two planes for any
sonogaphic abnormality, and the longest longitudinal diameter
was measured. Then color doppler was

turned on for easy

identification of the renal artery. Color box size was adjusted . The
angle of insonation was set at 60 or less during the study of the
aorta and renal arteries. The sample gate was placed in the
center of the arterial lumen, and the width of the gate was set as
2 to 5 mm. The PSV in the abdominal aorta was recorded at the
level of 1cm below the origin of the superior mesenteric artery.
Then, doppler traces was obtained from the distal segments of
renal artery near the hilum , as it is the easiest approach, at the
possibly smallest doppler angle, or Doppler spectra was elicited ,
and the PSV will be recorded.

3.5. Study Measures


Measures that were evaluated in this study are:
Measures drawn by asking the patient:
Age,

gender,

occupation,

chronic

morbidities,

duration

of

hypertension, the last laboratory test for renal function.


Measures drawn from ultrasound examination for both right
and lift kidneys:

48

Kidney size, renal artery PSV, renal artery RI, aortic PSV, renal
aortic ratio, spectral waveform, and any gray scale or color
doppler abnormalities found.

3.6. Data Collection


Via data collection sheets designed to contain all study measures.

3.7. Data Analysis


It was carried out using statistical package for social sciences
computer

program

(SPSS).

The

associations

between

the

conclusion's different results and measurements are tested using


chi-square test; level of significance 0.05 was used.

3.8. Data presentation


Tables and figures.

3.9. Time line


Duration of this study was 7 months from (Feb 2014 Aug 2014) .

3.10. Ethical Considerations


A verbal consent was submitted from all patients for the
research participation . Justice and human dignity was maintained
on treating all patients.
49

3.11. Limitations of the Study


Limited

availability

of doppler ultrasound machines and well

trained personnels .

Chapter Four
Results
50

Chapter Four
4.Results
Frequency of renal artery stenosis is 2% among studied cases,
as shown in table (4.1) and figure (4.1).
22% of studied case are under the age of 20, 30% are 20-40
years old, 41%are 40-70 years old, and 7% are older than 70 , as
shown in table (4.2) and figure (4.2).
51% are males, and 49% are females, as shown in table (4.3)
and figure (4.3).
27% are housewives, 22% teachers, 17% employers, 11% free
workers ,and 23% are students. , as shown in table (4.4) and
figure (4.4).
51

Hypertension is newly discovered in 39% of cases, 35% had it


for less than 10 years, and 26% had it for more than 10 years, as
shown in table (4.5) and figure (4.5).
55% have no associated comorbidities, 20% have diabetes,
18% have ischemic heart disease, and 7% have both diabetes and
ischemic heart disease, as shown in table (4.6) and figure (4.6).
Renal function test is normal in 55% of cases, just abnormal in
35%, and 10% have end stage renal disease. , as shown in table
(4.7) and figure (4.7).
The mean length is 8.9 cm for Rt kidney, and 9.4 cm for Lt
kidney, as shown in table (4.8) and figure (4.9) and (4.9).
The mean value of peak systolic velocity is 41.3 cm/s for Rt
renal artery, 48.7 cm/s for Lt renal artery, as shown in table (4.8)
and figure (4.10) and (4.11).
The mean resistive index value is 0.58 in Rt renal artery, and
0.56 in Lt renal artery, as shown in table (4.8) and figure (4.12)
and (4.13).
The mean renal artery PSV to aorta PSV ratio is 1.06 in Rt renal
artery, and 1.19 in Lt renal artery, as shown in table (4.8) and
figure (4.14) and (4.15).
100% of spectral doppler waveform are normal, no
Barvus/tardus waveform seen, as shown in table (4.9) and figure
(4.16).
75% of cases have no other kidney sonographic abnormalities,
18% have simple cysts, 7% have poor corticomedullary
differentiation, as shown in table (4.10) and figure (4.17).
Crosstabulation of renal artery stenosis with the other study
variables, the two affected cases are males, with p value = 0.161
as shown in table (4.12) and figure (4.19). in the age group of 2052

40, with p value = 0.190 as shown in table (4.11) and figure


(4.18).
They were referred with newly discovered hypertension, with p
value = 0.203 as shown in table (4.13) and figure (4.20).
No other kidney sonographic abnormality found during the scan,
with p value = 0.712 as shown in table (4.16) and figure (4.23).
One of them has normal renal function test and the other has
abnormal test, with p value = 0.842 as shown in table (4.15) and
figure (4.22).
, and no associated comorbidities, with p value = 0.644 as shown
in table (4.14) and figure (4.21).
Crosstabulation of the duration of hypertension and Rt and Lt
renal artery RI is as shown in table (4.17) and (4.18), figure (4.24)
and (4.25). p value = 0.000 .
Crosstabulation of the renal function test and Rt and Lt renal
artery RI is as shown in table (4.19) and (4.20), figure (4.26) and
(4.27). p value = 0.000 .

Table 4.1 :Renal artery stenosis


Valid

yes
no

Frequency
2
98

Percent
2.0
98.0

Valid Percent
2.0
98.0

100

100.0

100.0

Total

53

Cumulative Percent
2.0
100.0

Figure 4.1 : Renal artery stenosis

Table 4.2 :age

Valid

less than 20
20-40
40-70
more than 70

Frequency
22
30

Percent
22.0
30.0

Valid Percent
22.0
30.0

41

41.0

41.0

93.0

7.0

7.0

100.0

100

100.0

100.0

Total

54

Cumulative Percent
22.0
52.0

Figure 4.2 : Age

Table 4.3 : gender


Frequency
Valid

male

Percent

Valid Percent

Cumulative Percent

51

51.0

51.0

51.0

49

49.0

49.0

100.0

100

100.0

100.0

female

Total

55

Figure 4.3: gender

Table 4.4 :Occupation

Valid

housewife
teaecher

Frequency
27
22

Percent
27.0
22.0

Valid Percent
27.0
22.0

employee

17

17.0

17.0

66.0

free worker

11

11.0

11.0

77.0

student

23

23.0

23.0

100.0

100

100.0

100.0

Total

56

Cumulative Percent
27.0
49.0

Figure 4.4 : occupation

Table 4.5 : HTN duration

Valid

newly discovered
less than 10 years
more than 10 years

Frequency
39
35

Percent
39.0
35.0

Valid Percent
39.0
35.0

Cumulative Percent
39.0
74.0

26

26.0

26.0

100.0

100

100.0

100.0

Total

57

Figure 4.5 : HTN duration

Table 4.6 :co mrbidities

Valid

none
DM
IHD
DM + IHD

Frequency
55
20

Percent
55.0
20.0

Valid Percent
55.0
20.0

18

18.0

18.0

93.0

7.0

7.0

100.0

100

100.0

100.0

Total

58

Cumulative Percent
55.0
75.0

Figure 4.6 : co morbidities

Table 4.7 : RFTs


Frequency
Valid

Percent

Valid Percent

Cumulative Percent

normal
abnormal
ESRD

55

55.0

55.0

55.0

35

35.0

35.0

90.0

10

10.0

10.0

100.0

100

100.0

100.0

Total

59

Figure 4.7 : RFTs

Table 4.8 : statistics of doppler values and kidney lengths

60

61

Figure 4.8 : Rt kidney length (cm)

Figure 4.9 : Lt kidney length (cm)


62

Figure 4.10 : Rt kidney PSV (cm/s)

Figure 4.11 : Lt kidney PSV (cm/s)


63

Figure 4.12 : Rt kidney RI

Figure 4.13 : Lt kidney RI


64

Figure 4.14 : Rt kidney R/A ratio

Figure 4.15 : Lt kidney R/A ratio


65

Table 4.9 : spectral waveform

Frequency
Valid

Percent

Valid Percent

Cumulative Percent

normal

Barvus/t
ardus
wave

100

100.0

100.0

100.0

100.0

Figure 4.16 : spectral waveform

66

Table 4.10 :other sonographic abnormalities


Frequency
Valid

none
simple cyst
poor CMD
Total

Percent

Valid Percent

Cumulative Percent

75

75.0

75.0

75.0

18

18.0

18.0

93.0

7.0

7.0

100.0

100

100.0

100.0

Figure 4.17 : other sonographic abnormalities

67

Table 4.11 :

age * Renal artery stenosis Cross

tabulation
Renal artery stenosis
yes
age

Total

no

less than 20
20-40
40-70

0
2

22
28

22
30

41

41

more than 70

98

100

Total

P value = 0.190

Figure 4.18 :

age * Renal artery stenosis Cross tabulation


68

Table 4.12 : gender * Renal artery stenosis Crosstabulation


Count
Renal artery stenosis
yes
gender

male
female

Total

Total

no
2

49

51

49

49

98

100

P value = 0.161

Figure 4.19 : gender * Renal artery stenosis Crosstabulation

69

Table 4.13 :HTN duration * Renal artery stenosis Crosstabulation


Count
Renal artery stenosis
yes
HTN
duration

newly discovered

Total

no
2

37

39

less than 10 years

35

35

more than 10 years

0
2

26
98

26
100

Total

P value = 0.203

Figure 4.20 :HTN duration * Renal artery stenosis


Crosstabulation
70

Table 4.14 :co mrbidities * Renal artery stenosis Crosstabulation


Count
Renal artery stenosis
yes
co mrbidities

Total

no

none

53

55

DM

20

20

IHD

18

18

DM + IHD

0
2

7
98

7
100

Total

P value = 0.644

71

Figure 4.21 :co mrbidities * Renal artery stenosis


Crosstabulation

Table 4.15 :RFTs * Renal artery stenosis Crosstabulation


Count
Renal artery stenosis
yes
RFTs

normal
abnormal
ESRD

Total

Total

no
1
1

54
34

55
35

10

10

98

100

P value = 0.842

72

Figure 4.22 :RFTs * Renal artery stenosis Crosstabulation


Table 4.16 :other sonographic abnormalities * Renal artery
stenosis Crosstabulation
Count
Renal artery stenosis
yes
other sonographic
abnormalities

none
simple cyst
poor CMD

Total

Total

no
2

73

75

18

18

98

100

P value = 0.712

73

Figure 4.23 :other sonographic abnormalities * Renal artery


stenosis Crosstabulation

Table 4.17: HTN duration* Rt renal artery RI Crosstabulation

P value = 0.000

74

Figure 4.24: HTN duration* Rt renal artery RI Crosstabulation


Table 4.18: HTN duration*Lt renal artery RI Crosstabulation

P value = 0.000

75

Figure 4.25: HTN duration* Lt renal artery RI Crosstabulation

Table 4.19: RFTs*Rt renal artery RI Crosstabulation

P value = 0.000

76

Figure 4.26: RFTs* Rt renal artery RI Crosstabulation


Table 4.20: RFTs *Lt renal artery RI Crosstabulation

P value = 0.000

77

Figure 4.27: RFTs* Lt renal artery RI Crosstabulation

Chapter Five
Discussion, Conclusion,
Recommendations, References &
Appendices

78

Chapter Five
5.1. Discussion
Frequency of renal artery stenosis is 2% among studied cases,
which is comparable to the already known prevalence of renal
artery stenosis in unselected population. (2)
Correlating renal artery stenosis with the other study variables,
the two affected cases are males, in the age group of 20-40 which
is in favor of fibromuscular dysplasia as etiology rather than
atherosclerosis.
They were referred with newly discovered

hypertension,

Which reflects high level of awareness from both the patients and
clinicians.
Spectral doppler wave form was normal even in patients
suffering from renal artery stenosis, because the artery was
sampled just proximal to the kidney in most of cases, where the
Barvus/tardus wave is suspected in the renal parenchymal vessels
at interlobar arteries level.
No other kidney sonographic abnormality found during the
scan, that is because of early presentation before end stage renal
failure is reached or hemodialysis is needed, and the age group of
patients is not the age of the simple renal cysts.
One of them has normal renal function test and the other has
abnormal test, and no associated comorbidities. This finding is
79

far different from what resulted in the previously mentioned


studies which showed higher prevalence of renal artery stenosis
in groups like advanced ages, patients with type 2 diabetes, and
patients undergoing catheter coronary angiography, which are all
strongly associated with atherosclerosis. This contrast in findings
can be explained knowing that only 7% of study population were
over 70 years, and the diseased renal arteries are more likely to
be caused by fibromuscular dysplasia.
Crosstabulation of
showed

RI value with duration of hypertension

statistically significant association, p value = 0.000 .

Also, crosstabulation of RI value against renal function showed


statistically significant association, p value = 0.000. These
findings match what mentioned before in the local and Japanese
studies that found increased RI values in diabetic patients with
poor renal function, That is explained knowing that, hypertension
is associated with a more rapid loss of renal function. This may be
due to transmission of higher pressures into the glomerulus as
afferent renal artery resistance fails to limit transmission of higher
systemic

pressures

into

the

nephron.

Higher

glomerular

transcapillary pressures and flows injure glomerular cells by


several mechanisms, ultimately leading to glomerulosclerosis,
which is a progressive process.(1)

80

5.2. Conclusion
Frequency of renal artery stenosis using duplex sonograghy as
screening tool

is 2% among hypertensive patient in Khartoum

population.
Cases seen are most likely caused by fibromuscular dysplasia
rather than atherosclerosis.
Renal artery stenosis affect young age groups is not associated
with other comorbidities , as diabetes or ischemic heart disease.
Renal artery stenosis affect young age groups is not associated
with renal function abnormality.
Sonographic appearance of kidneys suffering from renal artery
stenosis is likely to be normal in young patients.
RI of the renal artery is significantly affected by the
function.
81

renal

RI of the renal artery is significantly affected by the duration of


hypertension.

5.3. Recommendations
This study emphasizes the role of doppler ultrasound as the
first line investigation for screening and diagnosis of renal artery
stenosis due its advantages over the other imaging modalities.
Renal artery stenosis is fatal disease with serious
complications as stroke, heart attacks, and other morbidities that
can be avoided by raising the awareness of the importance of
early screening of suspected cases.
As atherosclerosis can also cause renal artery stenosis, patients
with systemic atherosclerosis should be screened and followed up
with renal artery doppler.

82

Universal protocols of renal artery examination should be


followed closely to guarantee accurate and valid diagnosis. This
means to scan the

kidneys carefully with both gray-scale and

doppler modes, and not to ignore any measureable doppler value,


especially the ratio of renal artery systolic velocity to aorta.
The operators should be keen to improve their performances
through continuous training, and by keeping updated with new
protocols and medical discoveries.
Doppler ultrasound machines should be widely available in all
hospitals, with regular quality assurance programs.
Archiving systems in radiology departments should be
computerized and properly designed to give accurate and
detailed information that can be advantageous for both clinicians
and researchers.
Renal artery stenosis is a rich field that still needs meticulous
researching with larger samples and expanded time for more
generalizable results.

References
1.Thomas M. Habermann , Amit K. Josh . 1 st ED . Mayo Clinic
Internal Medicine Concise Book . Mayo Clinic Scientific Press;
USA:2008. Pages(458-463)
2.W. Schaberle. Ultrasonography in Vascular Diagnosis A Therapy
Oriented Text Book and Atlas. Springer; Germany:2004.pages
(270-283)
83

3.World Health Statistics 2013. By World Health Organization.


4.Soumeya M. Sherif, M. Elbaghir K. Ahmed, Mamoun M. Homaida.
Prevalence of Hypertension in Urban Community in Sudan.
Khartoum Medical Journal.(2008)vol.01 No. 02 pp72-74.
5.Sarra Elamin, Wafaa Obaid, Hasan Abu Aisha. Renal
Replacement Therapy in Sudan 2009. Arab Journal of Nephrology
and Transplantation. 2010 may3; (2):316.Carol M. Rumak, Stephani R. Wilson, J.W. Charboneau. D. Levine.
4th ED. Diagnostic Ultrasound. Mosby; USA: 2011.pages(394-396)
(475-482)
7. Bright R. Tubular view of the morbid appearances in 100 cases
connected with albuminous urine: With observations. Guys Hosp
Rep. 1836;1:380400
8. Tigerstedt R, Bergman PG. Niere und Kreislauf. . Skand Arch
Physiol. 1898;8:223271.
9. Goldblatt H, Lynch J, Hanzal RF, Summerville WW. Studies on
experimental
hypertension, I: the production of persistent elevation of systolic
blood pressure by
means of renal ischemia. J Exp Med. 1934;59(3):347-379.
10. Pallone TL, Zhang Z, Rhinehart K. Physiology of the renal
medullary
microcirculation. Am J Physiol Renal Physiol. 2003;284(2):F253266.
11. Mattson DL. Importance of the renal medullary circulation in
the control of sodium excretion and blood pressure. Am J Physiol
Regul Integr Comp Physiol. 2003;284(1):R13-27.
12. Cheung CM, Hegarty J, Kalra PA. Dilemmas in the
management of renal artery stenosis. Br Med Bull. 2005;73-74:3555.
13. Safian RD, Textor SC. Renal-Artery Stenosis. New England
Journal of Medicine.2001;344(6):431-442.
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85

14.

Ohta, Yuko; Fujii, Koji; Arima, Hisatomi; Matsumura,

Kiyoshi; Tsuchihashi, Takuya; Tokumoto, Masanori; Tsuruya,


Kazuhiko;

Kanai,

Hidetoshi;

Iwase,

Masanori;

Hirakata,

Hideki; Iida, Mitsuo, 2005, Increased renal resistive index in


atherosclerosis

and

diabetic

nephropathy

assessed

by

Doppler sonography, Journal of Hypertension. 23(10):19051911,

June

19th

2012,

URL:

www,

ncbinih,

gov,/pubmed/16148615.
15.
.Ala Mohammed Abd Elgyoum Mohamed Ahmed1,Abd
Allah

Mohammed

Jaber2,Amin

A.

E.

Elzaki3;

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Ultrasonography Of The Kidneys In Diabetic Patients, Asian


Journal

of

Medical

Radiological

Research

13(5):234-23,

10May 2013.
16.
Akram A. Saleh, MBBS, MRCP, Basem B. Bustami
Prevalence of renalartery stenosis in patients undergoing
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Jonathan Valabhji, Stephen Robinson, Claire Poulter,
Adam C.J. Robinson, Chantal Kong, Christoph Henzen,; P
revalence of Renal Artery Stenosis in
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3 :5 3 9543, 2000

Benjamin MM, Fezal P, Filardo G, and Stoler RC, the

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86

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Andersen UB , Borglykke A, and

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\
Appendix 1: Renal artery spectral doppler showing renal artery
stenosis, PSV 452.4 cm/s, RI 0.80, R/A ratio 9.45 in 25years male
with newly discovered HTN & abnormal renal function.

87

Appendix 2: Renal artery spectral doppler showing renal artery


stenosis, PSV 140.5 cm/s, RI 0.67, R/A ratio 4.01 in 32 years male
with with newly discovered HTN & normal renal function.

Appendix 3: Normal renal artery spectral doppler in 45 years


with less than 10 years HTN ,female presented with pulmonary
edema.

88

Appendix 4: Normal renal artery spectral doppler in 50 years


male with years with less than 10 years HTN & abnormal renal
function.

Appendix 5: Normal renal artery spectral doppler in 65years


male with more than 10 years HTN, ESRD, DM & IHD.

89

Appendix 6: Normal renal artery spectral doppler in 60 years


female with less than 10 years HTN & normal renal function.

Appendix 7: Normal renal artery spectral doppler in 38 years


male with less than 10 years HTN & normal renal function.

90

Appendix 8: Normal renal artery spectral doppler in 67years


male with more than 10 years HTN & normal renal function.

Appendix 9: Normal renal artery spectral doppler in 55years


female with less than 10 years HTN & normal renal function.

91

Appendix 10: Normal renal artery spectral doppler in 25years


female with newly discovered HTN & normal renal function.

Appendix 11: Normal renal artery spectral doppler in 72 years


male with ESRD & more than 10 years HTN.
.

92

Appendix 12: Normal renal artery spectral doppler in 45years


male with less than 10 years HTN & normal renal function.

Appendix 13: Normal renal artery spectral doppler in 40 years


male with less than 10 years HTN & normal renal function.

93

Appendix 14: Normal renal artery spectral doppler in 65years


male with more than 10 years HTN & abnormal renal function.

Appendix 15: Normal renal artery spectral doppler in 33years


male with newly discocered HTN & normal renal function.

94

Appendix 16: Normal renal artery spectral doppler in 48years


female with less than 10 years HTN & normal renal function.

Appendix 17: Normal renal artery spectral doppler in 36years


with newly discovered HTN & abnormal renal function.

95

Appendix 18: Normal renal artery spectral doppler in 59 years


male with less than 10 years HTN , DM & normal renal function.

Appendix 19: Normal renal artery spectral doppler in 35years


male with newly discovered HTN & abnormal renal function.

96

Appendix 20: Normal renal artery spectral doppler in 49 years


male with less than 10 years HTN & normal renal function.

Appendix 21: Normal renal artery spectral doppler in 22years


male with newly discovered HTN & abnormal renal function.

97

Appendix 22: Normal renal artery spectral doppler in 40 years


female with less than 10 years HTN & normal renal function.

Appendix 23: Normal renal artery spectral doppler in 60 years


male with more than 10 years HTN & normal renal function.

98

Appendix 24: Normal renal artery spectral doppler in 25years


female with newly discovered HTN & normal renal function.

Appendix 2 5: Normal renal artery spectral doppler in 50years


female with more than 10 years HTN & normal renal function.

99

Appendix 26: Normal renal artery spectral doppler in 44 years


male with less than 10 years HTN & normal renal function.

Appendix 27: Normal renal artery spectral doppler in 43years


male with less than 10 years HTN & abnormal renal function.

100

Appendix 28: Normal renal artery spectral doppler in 60years


male with more than 10 years HTN & normal renal function.

Appendix 29: Normal renal artery spectral doppler in 42years


female with less than 10 years HTN, DM & normal renal function.

101

Appendix 30: Normal renal artery spectral doppler in 72years


female with more than 10 years HTN , IHD & normal renal
function.

Data Collection Sheet


Age

Gender

Occupation

Co morbidities :
none
DM + IHD

DM

IHD

Duration of HTN :
newly discovered
< 10 years

>10 years

Renal function test :


102

normal

abnormal

ESRD

Doppler Values
Renal
PSV

Renal
RI

Aortic
PSV

R/A
Ratio

Renal
length

Rt
Lt

Spectral waveform :
Normal

Barvus / Tardus wave

Other sonographic or color doppler abnormalities:


None
others

simple cysts

103

poor CMD