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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 AP 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 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 9. 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.

3.2.Renal Circulation Anatomy and Physiology

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 (20-25%) 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. 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 . 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

3.3.Etiology of renal artery stenosis

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

3.4. 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 volumedependent 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 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

3.5.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 systolic-diastolic
bruit in the upper abdomen or flank. However, 50% of persons with renovascular
hypertension do not have this finding. 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, 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

3.6.Screening Tests
Duplex Ultrasonography will be discussed later.
3.6.1.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 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
3.6.2.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.
Historically, the intravenous pyelogram (IVP) was the mainstay screening
test for renovascular hypertension. For screening, radiographs that are taken at 1minute 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-to-pole diameter
of the smaller kidney); 2) delayed appearance of contrast medium in the collecting
system of the ischemic kidney; 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

3.6.3.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 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
3.6.4.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-angiotensin-aldosterone
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 can be influenced by
many factors that are difficult to identify and control, predictive accuracy is low.1
3.6.5.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
3.6.6.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
3.6.7.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
may be 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 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

3.7.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,
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, dye-induced 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-to-pole length of 8 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 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

3.8.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 in up to 50% of cases. Often, accessory or branch vessel
disease is not identified. The sensitivity and specificity are 75% to 80%.1

3.8.1.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. 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 wedgeshaped areas without color coding (high but artifact-free gain, low pulse repetition

3.8.2.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 end-diastolic
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 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

3.8.3.Doppler Interpretation
There are many proposed guidelines for Doppler interpretation. Proposed
parameters to assess for stenosis include the peak 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. False-negative 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 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 than in a smaller facility. Once the
program is mature, the study is financially viable and can result in improved
patient care .6

3.9.Previous 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).V
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%.178
A population based study about the prevalence of renal artery stenosis in subjects
with moderate to severe hypertension by Andersen UB , Borglykke A, and
Jorgensen T, examined 332 subjects aged 50-66 years using doppler ultrasound,
with blood pressure <160\100, found the prevalence to be 3.3% in the examined
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.
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%;
Karla et al. Kidney Int 2005, found the Prevalence of clinically manifested
atherosclerotic renal-artery stenosis in the Medicare population is 0.5% overall and
5.5% among patients with chronic kidney disease .
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.