Estimation of Frequency of Renal Artery Stenosis

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
III
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
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

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
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 :

68
Table 4.12 : gender * Renal artery stenosis Crosstabulation

Count
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
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
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
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
Count
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

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.
84
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;
Doppler
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
routine cardiac catheterization, Saudi Med J 2004; Vol. 25 (1):
52-54.
17.
Jonathan Valabhji, Stephen Robinson, Claire Poulter,
Adam C.J. Robinson, Chantal Kong, Christoph Henzen,; P
revalence of Renal Artery Stenosis in
Subjects With Type 2 Diabetes an Coexistent Hypertension,
Diabetes Care 2
18.
3 :5 3 9543, 2000
Benjamin MM, Fezal P, Filardo G, and Stoler RC, the
prevalence and risk factors of
renal
artery stenosis in
patients with resistant hypertension, 23(10):1905-1911, Feb

15th 2014.
86
19.
Andersen UB , Borglykke A, and
Jorgensen T, the
prevalence of renal artery stenosis in subjects with moderate

to severe hypertension, 33(15):1905-1811, 2001.
\
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

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

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

male with less than 10 years HTN & normal renal function.
90

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

91

female with newly discovered HTN & normal renal function.

male with ESRD & more than 10 years HTN.
.
92


93

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

male with newly discocered HTN & normal renal function.
94


with newly discovered HTN & abnormal renal function.
95

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

male with newly discovered HTN & abnormal renal function.
96


male with newly discovered HTN & abnormal renal function.
97


98

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


male with less than 10 years HTN & abnormal renal function.
100


female with less than 10 years HTN, DM & normal renal function.
101

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

Estimation of Frequency of Renal Artery Stenosis

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Alzaiem Al-Azhari University

Faculty of Graduate Studies and Scientific

Estimation of the Frequency of Renal Artery

A Thesis Submitted For Partial Fulfillment of the

Presented By : Dr. Walaa Ismail Musa

Supervisor : Dr. Suzan Omar Abd-Alla

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

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

preserve renal function, and prevent development of end-stage

The study emphasized the role of duplex sonography as a

angiotensin converting enzyme

angiotensin receptor blocker

digital substraction angiography

end diastolic velocity

maximum intensity projection

magnetic resonance angiography

plasma rennin average

PTRA percutaneous transluminal renal

partial oxygen pressure

PSV peak systolic velocity

T99m technetium 99 metastable

Causes of increased RI in renal arteries

Different sonographic criteria used for

Frequency of Renal Artery Stenosis

Frequency distribution of patients according to occupation

Normal vascular anatomy of the kidney

Frequency distribution of patients according to RFTs

other sonographic abnormalities * Renal artery

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

hypertension. Known secondary forms of hypertension account for

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

Renal artery stenosis is commonly caused by either

stenosis virtually always occur at the origins of the renal arteries

1.1.2. Screening Tests

resonance angiography, and spiral computed tomographic (CT)

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

1.1.3. importance of the study

This represents a considerable rise from 7.5% in

replacement therapy in Sudan revealed that hypertension was

ascertain even in patients with long standing hypertension.

1.2.2. Specific Objectives

In 1898 Tigerstedt and Bergman discovered that extract from the

The first successful experimental model of arterial hypertension

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

2.2.Renal Circulation Anatomy and Physiology

The kidneys play an essential role in maintaining a stable

juxtamedullary glomeruli form vasa recta capillaries that form

. Thus, the renal

circulation consists of two capillary beds connected in series by

2.3.Etiology of renal artery stenosis

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

FMD may involve other major arteries, commonly internal

2.4. Pathophysiology of Renovascular Hypertension

unilateral disease, the nonischemic kidney is subjected to

nonischemic kidney (in combination with other cardiovascular risk

2.5.Clinical Clues of Renovascular Hypertension

accelerated or malignant hypertension, or sudden worsening of

hypertension). Persons with cardiovascular risk factors (tobacco

Other physical clues are severe retinopathy of accelerated or

papilledema) or evidence of atherosclerotic occlusive disease in

eosinophiluria) help identify this disorder. In young persons who

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

distal main renal arteries or lesions in branch vessels (common