R evie w Paper
Renovascular Hypertension: An Update
William J. Elliott, MD, PhD
Renovascular hypertension, the most common
remediable cause of elevated blood pressure, is
a controversial topic, but most authorities agree
on several principles. The absolute risk of reno-
vascular hypertension for a specific patient can
be estimated using only clinical information,
thereby sparing many patients further expensive
and potentially dangerous evaluations. Patients
with a high absolute risk of renovascular hyper-
tension should have angiography only if they are
willing to undergo revascularization if warranted.
A screening test (captopril renography, Doppler
ultrasonography, magnetic resonance angiogra-
phy, or computed tomography) is recommended
for those with an intermediate absolute risk.
Angioplasty should be offered to patients with
fibromuscular dysplasia. Whether intensive medi-
cal therapy (including an angiotensin-converting
enzyme inhibitor or angiotensin II receptor block-
er) for atherosclerotic renovascular hypertension
is improved by angioplasty plus stent placement
may be answered by ongoing studies, the larg-
est of which may be the National Institutes of
Healthfunded Cardiovascular Outcomes in
Renal Atherosclerotic Lesions (CORAL) trial. J
Clin Hypertens (Greenwich). 2008;10:522533.
2008 Le Jacq
From the Department of Preventive Medicine, Rush
Medical College, Rush University Medical Center,
Chicago, IL
Address for correspondence: William J. Elliott, MD,
PhD, Department of Preventive Medicine, Rush
Medical College, Rush University Medical Center, 1700
West Van Buren, Suite 470, Chicago, IL 60612
E-mail: welliott@rush.edu
Received September 25, 2007;
revised February 5, 2008; accepted February 14, 2008
www.lejacq.com ID: 7788
522 THE Journal of Clinical Hypertension
I n most industrialized countries, renovascular
disease is the most common remediable cause
of elevated blood pressure (BP), especially among
older hypertensive patients.18 Although Goldblatt
and colleagues developed the animal model that
led to understanding its pathophysiology more
than 70 years ago,9 the diagnosis and manage-
ment of renovascular hypertension have markedly
changed over the last 40 years, due to more accu-
rate diagnostic procedures, more specific and effec-
tive antihypertensive medications, and the results
of randomized clinical trials.3,4,6,8 This article
reviews some of the current controversies regard-
ing risk assessment before screening tests, selective
use of angiography, and limitation of invasive but
potentially curative procedures to persons who are
most likely to benefit.
Definitions
Renovascular Hypertension vs Renal Artery Stenosis
Unlike most other cardiovascular and renal con-
ditions, renovascular hypertension can be diag-
nosed only retrospectively. Classically, renovas-
cular hypertension can be correctly and properly
diagnosed 6 to 12 weeks after an intervention (see
below), only if the BP is lower than it was before
the intervention, with the patient taking the same
or fewer antihypertensive medications. In contrast
to renovascular hypertension (which has a physi-
ologic basis for its diagnosis), renal artery stenosis
is an anatomic diagnosis. Classically, renal artery
stenosis was diagnosed when there was a >75%
narrowing of the diameter of a main renal artery
or >50% luminal narrowing with a poststenotic
dilatation. These criteria were based on planar
images derived from renal angiograms done in the
mid-1970s; typically, a 50% luminal narrowing is
the minimum in the current literature.
The distinction between renovascular hyper-
tension and renal artery stenosis has at least 3
important consequences. First, many older persons
VOL. 10 NO. 7 JUly 2008
have relatively advanced renal arterial stenoses on
angiography, but few have resistant hypertension.10
Second, surgical removal of a small kidney due to
presumed ischemic nephropathy (from renovascu-
lar hypertension) has been followed by normal BP
values in only about 25% of the patients in whom
it was attempted in the mid-1950s. Third, diagnos-
tic performance of screening tests for renovascular
hypertension are different from those for renal
artery stenosis, because the latter analysis usually
includes 2 arteries per person, whereas the former
is done based on responses in individual patients.
Subtypes of Renovascular Disease
Fibromuscular Dysplasia
Fibromuscular dysplasia (FMD) is a noninflam-
matory, nonatherosclerotic vascular disease that
preferentially affects small to midsized arteries.11
Although any vascular bed can be affected, it is
most common in the renal arteries (60%75%,
where it preferentially involves the distal two-thirds
of the main renal arteries). The etiology of FMD,
the most common cause of renovascular hyperten-
sion in young women (1530 years), is uncertain,
but it may be in part genetic. It has been associated
with female sex; cigarette smoking; ergotamine,
methysergide, and a1-antitrypsin deficiency; pheo-
chromocytoma, type IV Ehlers-Danlos syndrome,
Alports syndrome, cystic medial necrosis, neurofi-
bromatosis, and coarctation of the aorta (the latter
2 especially in children).
FMD is an important subtype of renovascular
hypertension for 2 reasons. Unlike atheroscle-
rotic disease, it rarely progresses to renal arterial
occlusion and/or ischemic nephropathy.4,11 Most
important, when found in the main renal arteries,
it responds extremely well to angioplasty without
stent placement. Most recent series indicate that
about 40% to 55% of such patients have their BP
normalized, with another 30% to 40% improved
after angioplasty. Because FMD occurs most com-
monly in young women, the prospect of saving
years of expensive drug treatment with successful
angioplasty is economically attractive.
Atherosclerotic Disease
Probably about 90% of current patients with reno-
vascular hypertension have atherosclerotic disease
as the underlying pathologic reason for the arterial
stenosis. This progressive, occlusive process typi-
cally narrows the ostium and proximal third of the
main renal artery, as well as the nearby aorta. As
with all other atherosclerotic vascular diseases, it
is found with increasing frequency with advancing
VOL. 10 NO. 7 JULY 2008
age and has the usual associated risk factors (dia-
betes, dyslipidemia, tobacco use, and history of
cardiovascular events).
Other (Less Common)
Causes of Renovascular Disease
On a population basis, Takayasus arteritis may be
the most important less common cause of renovas-
cular disease, especially in India or Japan. Renal
arterial aneurysms are a common finding with
medial fibroplasias but are often seen in saccular
forms (as large as 2 cm) at the bifurcation of the
renal artery. Rarer causes of renovascular disease
include nonstenotic, but quite long, aberrant renal
arteries, emboli generated during endovascular
procedures, aortic dissection, or kidneys that move
more than 7.5 cm while changing from supine to
erect posture.
Estimates of Prevalence and Risks
Traditionally, the prevalence of renovascular hyper-
tension was estimated to be 5% of all hypertensive
individuals, but it varied from <1% to >50%
depending on the populations characteristics. In a
population-based sample of claims from 1,085,250
Medicare beneficiaries in 1999 through 2001, the
incidence of atherosclerotic renovascular disease
was 3.7 per 1000 patient-years.12 FMD is more
common among young hypertensive women. In
the late 1980s, FMD represented 30% to 40% of
cases of renovascular hypertension at referral cen-
ters, but today it composes <10% of cases, as the
general population ages and atherosclerotic disease
becomes more prevalent.
The major risks of renovascular hypertension
are those associated with persistently increased
BP and with atherosclerotic disease, ischemic
nephropathy, and a high risk of cardiovascu-
lar events. Renovascular hypertension tends to
be relatively resistant to usual drug therapies;
administration of either an angiotensin-converting
enzyme (ACE) inhibitor or an angiotensin II
receptor blocker (ARB) can provoke acute renal
failure (characteristic of bilateral disease or steno-
sis of a solitary kidney). In this setting, recurrent
pulmonary edema can be a presenting symptom
of renovascular hypertension, and it frequently
improves or disappears after opening the artery.
Patients with FMD seldom sustain renal artery
occlusion or ischemic nephropathy, but this is a
major risk for patients with atherosclerotic disease
that often leads to end-stage renal disease.13 In a
series of 220 patients with atherosclerotic disease
followed by ultrasonography (US) to observe its
THE Journal of Clinical Hypertension 523
 natural history before cholesterol-lowering drugs
were widely used, progressive renal arterial steno-
sis was seen in 31% over 3 years, including 18%
of originally nonstenotic arteries, with eventual
occlusion in 9 of 295 arteries. For patients with
<60% stenosis originally, 28% progressed, as
compared with 49% in those with stenosis >60%.
In addition, progressive renal cortical atrophy
was noted in 21% of patients when the original
degree of renal arterial stenosis was >60%.14 In
the Cardiovascular Health Study, renal artery
stenosis (detected by duplex US in 6% of persons
aged 65 years) was associated with a 1.96-fold
increased risk of coronary events, independent of
baseline blood pressure.15 Since atherosclerosis
is a systemic disease, it is hardly surprising that
individuals with renal artery lesions have a higher
risk of cardiovascular events.16 In one study during
a 2-year period, cardiovascular events in patients
with newly diagnosed atherosclerotic renovascular
hypertension were about 4 times more common
than in the general population and were more than
10 times more common than adverse renal events,
including end-stage renal disease.12
Pathophysiology
Classically, the pathophysiology of renovascular
hypertension involves progressive stenosis of
the renal artery, leading to hypoperfusion of the
juxtaglomerular apparatus, increased release of
renin, and increased production of angiotensin
II. This leads to increases in sympathetic nerve
activity, intrarenal prostaglandin synthesis, and
aldosterone synthesis and decreased nitric oxide
production; most important for the develop-
ment of hypertension, a direct decrease in renal
sodium excretion results. This sequence has been
validated acutely, originally in Goldblatts dogs,
but the situation in chronic renovascular disease
is more complicated. Over time, the increased
plasma renin activity decreases as plasma volume
expands, especially when chronic kidney disease
is present. During the chronic phase, both BP
and intravascular volume can be reduced by
angiotensin II antagonists or by removal of the
arterial stenosis.
In some animal models, removal of the arte-
rial stenosis does not result in an abrupt or
complete decrease in BP, compared with that of
age-matched control animals. This phenomenon
may be important in humans, as revascularization
surgery has been more successful in lowering BP if
hypertension has been present for <5 years before
the operation.
524 THE Journal of Clinical Hypertension
Diagnostic Evaluation
Although the algorithm for evaluation of sus-
pected renovascular hypertension is controversial,
the Figure outlines a common approach. An initial
estimation of the absolute risk of renovascular
hypertension can be based solely on clinical clues.
Identifying an abdominal bruit is said to be the
most cost-effective of these. This is often a high-
pitched, holosystolic bruit with a short diastolic
componentunlike the bruit often heard in older
persons with an atherosclerotic aorta, which is usu-
ally a short rough systolic murmur. If the patient is
unwilling to accept surgery (should it be required,
even to repair a dissection or perforation during
angioplasty), medical management alone is advised.
Renal angiography can be performed in individuals
at high risk for renovascular hypertension. A sensi-
tive screening test can be offered to those with an
intermediate probability of renovascular hyperten-
sion. The result will dichotomize those who do not
need further testing (but only medical management)
and those who should have another test (including
angiography). The cutoffs for the latter 2 steps and
which screening test should be recommended for
most patients is debatable.5,17
Initial Risk Estimation
Many of the characteristics that distinguish indi-
viduals with renovascular compared with primary
hypertension (Table I) were identified during the
1970s in a study of 2442 hypertensive patients,
of whom 880 had renovascular disease (35%
of whom had FMD). Dutch investigators have
advanced a clinical prediction rule that they
derived from one cohort of patients, validated
in a separate cohort, and revalidated in a third
cohort of patients with drug-resistant hyperten-
sion (35 with and 145 without renovascular
hypertension).18 A nomogram provides the prior
probability of renovascular disease, from a sum
of the number of points assigned to aspects of
the individuals history, physical examination, and
simple laboratory studies. This method does not
incorporate the BP or serum creatinine response to
a renin-angiotensin blocker.
Screening Tests
Several reasonably accurate screening tests for
renovascular hypertension have been developed.
Some are based on physiologic parameters (eg,
renin activity or blood flow to each kidney),
some are more anatomically based (magnetic
resonance angiography [MRA], computed tomo-
graphic angiography [CTA]), and some combine
VOL. 10 NO. 7 JUly 2008
Figure. A diagnostic algorithm for renovascular hypertension. RAS indicates renal artery stenosis; ACE, angiotensin-
converting enzyme.
aspects of each (Doppler US, captopril scintigra-
phy [CS]). The sensitivity and specificity of several
of the older tests (eg, plasma renin activity, renal
vein renin determinations, technetium-99m dieth-
ylenetriamine pentaacetic acid [Tc99m-DTPA] renal
scan) are improved after acute administration of an
ACE inhibitor.
In 2001, Dutch investigators reported a selec-
tive overview of the worlds literature on the
performance of screening tests for renal artery
stenosis. This end point was chosen because many
studies (especially in MRA and CTA) report only
relationships between the arterial appearance in
the screening test and angiography (ie, analysis
per artery), rather than per patient (as would be
the case if renovascular hypertension were the end
point). They concluded that CTA and gadolinium-
enhanced MRA were the best tests.19 Three years
later, however, their prospective, multicenter, com-
parative study of these 2 modalities (vs angiogra-
phy) in 356 patients indicated that neither could
VOL. 10 NO. 7 JULY 2008
be recommended.20 An updated (19902006) sum-
mary of a more inclusive literature review of the
sensitivity and specificity of each of these screening
tests for renal artery stenosis is given in Table II
and is discussed below.21
Captopril Scintigraphy
Several agents (Tc99m-DTPA, 121I-hippurate, or
technetium-99m mercaptoacetyltriglycine [Tc99m-
MAG3, also known as Tc99m-mertiatide]) can
image the kidneys after an oral dose of captopril.
Although CS is now widely available, relatively
inexpensive, and simple to perform and consensus
criteria for its interpretation exist,22 the results of
CS are very heterogenous (P<108 by Riley-Day
test) across the worlds literature. Some of the vari-
ability may be due to different isotopes (eg, MAG3
is better for detecting bilateral disease), unusu-
al characteristics of included patients (decreased
accuracy may exist in blacks and individuals who
take calcium antagonists), or different diagnostic
THE Journal of Clinical Hypertension 525
 Table I. Clinical Clues to Renovascular Hypertension
Approximate Relative Risk
Characteristic (vs Primary Hypertension)
Abdominal bruit (high-pitched holosystolic with diastolic component) 5.0
Recent loss of BP control (or onset of hypertension) 2.0
Unilateral small kidney 2.0
Keith-Wagener-Barker grade III or IV optic fundi 2.0
History of accelerated/malignant hypertension 2.0
Unprovoked hypokalemia (potassium level <3.4 mEq/L) 2.0
Increase in serum creatinine level after ACE inhibitor or ARB therapy 1.8
No family history of hypertension 1.8
Atherosclerotic disease in another vascular bed 1.8
Elevated plasma renin activity 1.8
History of cigarette smoking 1.7
Recurrent pulmonary edema 1.5
Proteinuria 1.4
Older age (per decade of life) 1.2
Hypertension refractory to an appropriate 3-drug regimen 1.2
Abbreviations: ACE, angiotensin-converting enzyme; ARB, angiotensin II receptor blocker; BP, blood pressure.

Table II. Performance Characteristics (Weighted Averages of The Worlds Literature 19902006) and Advantages/Disadvantages of
4 Screening Tests for Renal Artery Stenosis
Screening Doppler Magnetic Resonance Computed Tomographic
Test Captopril Scintigraphy Ultrasonography Angiography Angiography
No. of 69 47 30 14
publications
No. of patients/ 5282 2653 1623 1225
arteries
Sensitivity 0.79 (0.271.00) 0.83 (0.171.00) 0.88 (0.541.00) 0.86 (0.631.00)
(range)
Specificity 0.82 (0.441.00) 0.82 (0.631.00) 0.88 (0.231.00) 0.94 (0.631.00)
(range)
Advantages Noninvasive, not Noninvasive, inexpensive, No iodinated contrast needed; Excellent image quality
expensive, may predict may predict BP results excellent image quality
BP results after after revascularization
revascularization
Disadvantages Less accurate in renal Operator-dependent; less Expensive; poor images with Expensive, time-consuming
impairment, bilateral useful in obesity, bowel stents or distal stenoses (eg, to process and interpret;
disease, obstructive gas, branch lesions, FMD FMD); overcalls moderate not widely available;
uropathy stenoses; risk of gadolinium- large amount of contrast
associated fibrosing sometimes needed
dermopathy
Abbreviations: BP, blood pressure; FMD, fibromuscular dysplasia.

criteria across studies. In addition, bilateral renal
arterial disease, obstructive uropathy, and an
elevated serum creatinine level (>2.0 mg/dL) all
reduce the accuracy of CS using Tc99m-DTPA, the
most commonly used isotope. Using patient-/artery-
weighted averages, this test is about 79% sensitive
(range, 27%100%) and 82% specific (range,
44%100%) for detecting renal artery stenosis.
Several retrospective analyses suggest that CS may
predict BP outcomes after revascularization. In
hypertensive patients with normal renal function,
CS had an overall sensitivity and specificity of
about 90% each for renovascular hypertension;
the mean positive predictive value in 291 patients
from 10 studies was 92%.23 Unfortunately, the
only prospective randomized clinical trial to date
(discussed below) showed no relationship between
CS and BP response following angioplasty.24 For
these and other reasons, CS is no longer recom-
mended as a screening test for renal artery stenosis
in the 2005 American College of Cardiology/
American Heart Association guidelines.4

526 THE Journal of Clinical Hypertension VOL. 10 NO. 7 JUly 2008

Doppler US
Duplex US provides both anatomic and physi-
ologic information by directly identifying renal
arteries (using B-mode US) and providing hemo-
dynamic measurements within them (Doppler flow
studies). However, Doppler US has even more vari-
able performance characteristics than CS (P<1014
by Riley-Day test). Some of its disadvantages
(time-consuming, operator-dependent, poor-qual-
ity images due to obesity or overlying bowel gas)
can be overcome by scanning patients in the fasted
state, after a bowel preparation similar to that
undertaken before colonoscopy. Most reports of
Doppler US use 50% stenosis as the lower limit
of detection, since distinguishing between 50% to
69% and 70% stenosis is often difficult. Doppler
US has about 83% sensitivity (range, 17%100%)
and 90% specificity (range, 63%100%) for renal
artery stenosis. The most important feature of
successful Doppler US may be the renal resistive
index. In several (but not all) series, values <80
mm Hg have predicted improved BP following
revascularization.25 This observation has not yet
been validated in a randomized clinical trial. A
decision analysis (based on 74 patients in Quebec)
suggested that Doppler US is more cost-efficient
but less sensitive than MRA.26
Magnetic Resonance Angiography
Twenty-nine studies have compared MRA, typically
done today with phase contrast and/or gadolinium
enhancement, with renal angiography (Table II).
In the 2001 review of Vasbinder and associates,19
gadolinium-enhanced MRA and CTA had identical
and nearly perfect performance characteristics, but
the prospective study reported by the same group
in 2004 indicated that both interobserver variation
and sensitivity were much poorer than previously
noted.20 Their enrolled population had a high
prevalence of FMD (36%), which typically has
stenoses in the distal two-thirds of the renal artery,
an area not well visualized by the MRA technique.
Across all studies, MRA had a sensitivity of about
88% (range, 54%100%), a specificity of about
88% (range, 23%100%), and no significant inho-
mogeneity (P=.12). MRA was more accurate than
CS or US (each vs angiography) in 41 patients with
a 75% prevalence of renal artery stenosis,27 as well
as in 58 patients with a 77% prevalence of disease
(by transstenotic pressure gradient) compared with
CS, US, and CTA.28
Most of the technical challenges related to image
acquisition (eg, duration of breath holding), con-
trast injection, and patient positioning have now
VOL. 10 NO. 7 JULY 2008
been overcome. Its major advantages include excel-
lent image quality, utility in patients with advanced
renal impairment, and no need for potentially
nephrotoxic radiocontrast. Nephrogenic fibrosing
dermopathy is a very rare but serious consequence
of gadolinium infusions; some institutions pro-
hibit gadolinium administration without dialysis
for patients with stage 3 or higher chronic kidney
disease. Other limitations of MRA in the renal bed
include its expense; claustrophobia (said to affect
about 10% of patients); a tendency to overestimate
moderate (ie, 40%69%) stenoses; the need for
carefully timed intravenous injection of gadolini-
um; reduced accuracy in small, branch, and distal
renal arteries; attenuation of signal by indwelling
stents; and lack of functional information in the
results.
So far, only a single study has compared out-
comes after angioplasty based on MRA measure-
ments before the procedure.29 Despite unusual
criteria for a successful angioplasty (reduction
in diastolic BP >15% and/or reduction in serum
creatinine >20%) and stratification of the results
based on normal renal volume and a calcu-
lated renal flow index, the authors reported that
MRA had a 91% sensitivity and a 67% specificity
for predicting outcomes in their 23 patients. This
experience awaits replication by others. In a recent
cost-utility analysis, MRA led to the lowest direct
costs of any primary screening test if the prevalence
of renal artery stenosis in the tested population was
>20%, although essentially any strategy involving
successful revascularization saved more lives than
did medical treatment alone.30
Computed Tomographic Angiography
The newest common screening test is CTA, which
requires intravenous radiocontrast dye and more
time and effort in reconstructing 3-dimensional
images of the renal arteries. CTA had nearly
perfect performance characteristics in the origi-
nal analysis of Vasbinder and associates.19 Even
with the disappointing results in their prospective
study and much better performance in subsequent
reports, its overall sensitivity is about 86% (range,
63%100%), with a specificity of about 94%
(range, 63%100%). Only about 24% of the
significant inhomogeneity (P<.0001) across the
14 reported studies could be attributed to the pro-
spective study of Vasbinder and associates20; nearly
all of the remainder is due to 4 studies that report
nearly perfect correlation with renal angiography.
CTA is not yet as widely available as the other
screening tests, and so far it has not been correlated
THE Journal of Clinical Hypertension 527
 with BP-lowering outcomes after intervention. It
requires a good deal of computer technology and
programming expertise to identify all possible non-
planar arterial segments, so the time to reconstruct
and interpret images is longer than other screen-
ing tests. The volume of intravenous contrast that
is necessary to obtain good images is a concern.
Like MRA, CTA is not quite as accurate in small,
branch, or distal renal arteries, and claustrophobic
patients are uncomfortable. Indwelling stents are
not as big a concern as they are with MRA. Cost-
effectiveness calculations have not yet been done
for CTA, but it is likely that they should be simi-
lar (if a bit more expensive) than those done for
MRA. A urine CT attenuation ratio (left/right
density, in Hounsfield units, of proximal ureters or
renal pelvis obtained 45 minutes after injection
of contrast) >1.22 had a specificity and sensitivity
of 95% and 96%, respectively, in 28 patients with
angiographically proven renal artery stenosis, as
compared with 48 controls.31
Angiography
The gold standard for the diagnosis of renal
artery stenosis has long been renal angiography.
Unfortunately, it provides no functional informa-
tion about renal excretory function and carries
the risks of anaphylactoid shock, radiocontrast-
induced renal failure, and complications related
to vascular access. Individuals with a very high
absolute risk (typically 70%) of renovascular
hypertension should proceed directly to renal
angiography, rather than have an imperfect screen-
ing test, because the clinician would likely regard
any normal screening test as a false-negative and
recommend angiography anyway.
Intravenous digital subtraction renal angiography
was developed in the early 1980s to avoid arterial
puncture and the risks associated with it. Although
this technique cannot be followed as quickly by
angioplasty (because the contrast is delivered very
quickly into a peripheral vein), the delay can allow
for discussion as to whether revascularization is
truly appropriate (see below). Today, few measure
pressure gradients across apparent stenoses found
after intra-aortic renal angiography; instead, intra-
vascular ultrasonographic probes (especially for
FMD32) or (more commonly) guide wires precede
angioplasty catheters. A recent study of 17 patients
showed better prediction with renal fractional flow
reserve (measured after papaverine injection) than
translesional pressure gradients.33
One of the major controversies in renovascu-
lar hypertension today is the expanding role of
528 THE Journal of Clinical Hypertension
cardiologists in the fortuitous diagnosis and
subsequent immediate, catheter-based manage-
ment of renal artery stenosis.7,10,17,34 Much of
the 3.9-fold increase in Medicare claims for
renal artery revascularization between 1996 and
2000 has been attributed to cardiologists doing
drive-by renal arterial injections after coronary
angiography. So far, only one group has stratified
patients undergoing cardiac catheterization by cri-
teria that might put them at risk for renovascular
hypertension.35 These included (1) severe athero-
sclerosis, (2) severe or resistant hypertension, (3)
unexplained renal impairment, and (4) history of
acute pulmonary edema. They found that 39% of
their 837 patients had renal atherosclerosis, with
14% having stenosis 50% and 7% having steno-
sis 70%. The latter group was more likely to be
older and female and to have poorer renal func-
tion, higher BP levels, and carotid arterial disease.
Although this report carefully avoids mention of
whether any patient underwent renal angioplasty,
the authors intend to follow these patients for car-
diovascular and renal complications, which will
add to our knowledge of the natural (or postint-
ervention) history of patients with fortuitously
discovered renal artery stenosis, which may have
a different prognosis than disease discovered after
a premeditated search.
Although indications for renal angiography
during and after cardiac catheterization have
been proposed,10 many have questioned whether
it should be done. Two reports suggest little need
for the procedure. In a series of 68 patients with
renal artery stenosis found during aortography
done for other reasons at the Mayo Clinic, there
was no change in BP, an increase in antihyperten-
sive medications from 1.6 to 1.9 per patient, and
only a slight increase in serum creatinine (1.4 to
2.0 mg/dL) during 39 months of medical manage-
ment alone.36 In a multicenter British experience
involving 85 patients with incidentally discovered
renal artery stenosis, few required renal revas-
cularization, and 24 of the 27 deaths during 2
years of follow-up were unrelated to the renal
arteries.37 The real hazards associated with stent
placement (atheroemboli, dissections, thrombo-
sis, and renal failure) must be weighed against
the very controversial but potential benefits on
BP, progressive renal disease, and/or recurrent
pulmonary edema.4,7,10,34,38 It is not yet clear that
renal artery stenosis discovered fortuitously has
the same response to therapy as one found after
an intensive, premeditated search based on prior
probabilities.
VOL. 10 NO. 7 JUly 2008
Table III. Factors Influencing Selection of Patients for
Revascularization
Favorable Response After Revascularization
Recurrent flash pulmonary edema
Renal resistive index <80 mm Hg by Doppler
ultrasonography
Progressive, ongoing decline in renal function
Recent institution of dialysis in a patient with suspected
ischemic nephropathy
Acute, reversible increase in serum creatinine level after
angiotensin-converting enzyme inhibitor or angiotensin II
receptor blocker
Refractory hypertension despite an appropriate 3-drug
regimen
No Favorable Response After Revascularization
Blood pressure <140/90 mm Hg on <3 antihypertensive
drugs
Normal renal function
Renal resistive index 80 mm Hg by Doppler
ultrasonography
History or clinical evidence of cholesterol embolization
Heavy proteinuria (>1 g/d)
>10 Years history of hypertension
Unilateral small kidney (<7.5 cm in length)
Renal artery stenosis <70%
Therapy
Fibromuscular Dysplasia
Currently, angioplasty (alone) is the treatment of
choice for fibromuscular dysplasia. Technical suc-
cess and 1-year restenosis rates vary between 83%
and 100% and 5% and 11%, respectively.3,11 In
11 large series, 77% of 506 patients who had
primary angioplasty had either normalization or
improvement in BP.11,39 A shorter duration of
hypertension, younger age, and a lesion in a main
renal artery predict success.11 In a 7-year follow-
up, 34% of patients required repeat angioplasties,
sometimes years after an originally successful
procedure.39
Atherosclerotic Renal Artery Stenosis
Three major treatment options exist: surgical
revascularization, angioplasty with or without
stenting, or medical management. A recent sys-
tematic review of these concluded,38 The evi-
dence from direct comparisons of interventions
is sparse and inadequate to draw robust conclu-
sions. Some factors that can assist decision mak-
ing with an individual patient are given in Table
III. Whenever medical management is ineffective
in controlling BP or a progressive decline in renal
function occurs, revascularization can be more
strongly considered.40
VOL. 10 NO. 7 JULY 2008
Surgical Revascularization
Surgical revascularization for renal artery steno-
sis is currently less popular than angioplasty
with or without stent placement. However,
many surgeons assert that angioplasty may either
only postpone the definitive procedure, or,
worse, require an emergency operation if the
angioplasty goes awry. It is therefore useful and
customary to arrange surgical backup when
scheduling renal angiography with possible
angioplasty. Several experienced surgical teams
have reported an 80% to 90% rate of cured
or improved BP after an operation, but some
used softer end points (eg, a reduction in the
number of antihypertensive pills, but no change
in BP). Patients with normal renal function fare
better than those with reduced kidney function.
A recent series of 247 patients reported similar
outcomes whether open surgical or percutaneous
revascularization was performed.41 Traditional
aortorenal bypass and renal endarterectomy
are currently less popular than bypasses from
nonaortic donor (splenic, celiac, mesenteric, or
hepatic arterial) sites. These newer and more
elaborate procedures limit manipulation of the
diseased aorta and minimize atheroembolism at
the expense of a somewhat higher perioperative
mortality rate (2%6%). Most of the deaths are
related to graft failure or other complications of
widespread atherosclerotic vascular disease.
Angioplasty
Angioplasty (without stent placement) for ath-
erosclerotic disease has been less successful than
for FMD. In a review of large series of adults
undergoing renal angioplasty through 1995, only
65% of 1664 procedures resulted in normalized
or improved BP. About 19% were technical fail-
ures, and the restenosis rate at 1 year was about
13%. Less success occurred after angioplasty
of ostial lesions, sequential stenoses of a single
artery, or stenoses in multiple renal arteries to
the same side.6
The results of uncontrolled series reporting
renal angioplasty to preserve renal function are
difficult to interpret, due to lack of a comparable
control group. Overall, most large series report
little change in serum creatinine concentration or
other measures of renal function after angioplasty
(compared with preprocedure), although this
may well be due to about the same proportion of
patients who experience deteriorating renal func-
tion as those who improve.
THE Journal of Clinical Hypertension 529
 Angioplasty Plus Stent Placement
The addition of an expandable stent to balloon
angioplasty in the renal arterial bed has many
theoretical advantages, particularly in locations at
high risk for restenosis. Stent placement reduces or
resolves complications due to local dissection, pre-
vents elastic recoil (thought to be involved in acute
restenosis and thrombosis) and nearly eliminates
pressure gradients across lesions after angioplasty.
Because of these advantages, many operators now
prefer to place a stent whenever possible in the
renal arterial bed, despite the paucity of published
comparative data and the relatively short follow-
up available since its introduction. In a random-
ized trial of angioplasty plus stent placement vs
angioplasty alone in 84 patients with ostial lesions,
restenosis was much less common after 6 months
in those receiving stents (25% vs 70%), but there
were no differences across groups in BP or dete-
rioration in renal function. About a third of the
patients had major complications related to the
procedure.42
The largest experience with renal artery stent
placement comes from a registry of 1058 patients
followed for at least 6 months.43 Technical suc-
cess was universal; overall, there was a significant
decline in BP (16829/8415 to 14721/7812 ment, which has gradually fallen into disfavor, and
mm Hg; P<.05), a slight decrease in antihyper-
tensive medications per patient (2.4 to 2.0), and
improved renal function (serum creatinine changed
from 1.71.1 to 1.30.8 mg/dL) during a 4-year
follow-up, during which the overall mortality was
26%, which validates the high mortality risk in
persons with a documented atherosclerotic bur-
den. Other smaller and more recent reports show
similar results, although about the same number
of patients experience deteriorating renal func-
tion as improve after the procedure. Restenosis
rates vary between 10% and 30% (depending on
length of follow-up). Stent placement may have
special benefits in renovascular hypertension with
deteriorating (as opposed to abnormal but stable)
renal function.
Medical Management
Intensive therapy to control all atherosclerotic
risk factors (eg, antihypertensive drugs, aspirin,
3-hydroxy-3-methylglutaryl coenzyme A reductase
inhibitors, smoking cessation, and glycemic con-
trol) can be universally recommended for all
patients with renovascular disease. Without thera-
py, the long-term prognosis is at least as poor for
these patients as for diabetics and patients with a
previous myocardial infarction.16
530 THE Journal of Clinical Hypertension
The major concern about intensified antihyper-
tensive drug therapy is the risk of acute deteriora-
tion in renal function that sometimes occurs when
an ACE inhibitor or ARB is added to the regimen.
These drugs are effective in reducing BP in 86% to
92% of patients with renovascular hypertension
(most commonly in combination with a diuretic
and a calcium antagonist) and in the earliest pub-
lished experience, require discontinuation in only
about 5% during the first 3 months. The increase
in serum creatinine values typically reverts to
baseline after stopping the ACE inhibitor or ARB;
better BP control, despite an acute deterioration
in renal function after treatment with an ACE
inhibitor or ARB, can be an indication for renal
revascularization.
Clinical Trials and
Meta-Analyses Thereof
Several clinical trials related to therapy of reno-
vascular hypertension have been organized, but
crossovers, other confounders, and the continuing
evolution of what is considered state-of-the-art
treatment protocols complicate their interpreta-
tion. The latter problem especially affects early
trials involving angioplasty without stent place-
more recent studies in which differential use of
ACE inhibitors or ARBs occurred across random-
ized arms.38 The most recent systematic review of
management strategies found no good quality
studies, and only 4 (3 of which were cohort stud-
ies) with high applicability.38 The absence of
solid clinical trial data comparing angioplasty plus
stent placement with maximal medical therapy
was one of the major reasons for the Stent for
Atherosclerotic Ostial Stenosis of the Renal Artery
(STAR) study44 in Holland, governmental fund-
ing of the Angioplasty and Stent for Renal Artery
Lesions (ASTRAL) trial in Great Britain,45 and
the Cardiovascular Outcomes With Renal Artery
Lesions (CORAL) trial in the United States.46
The 3 randomized trials comparing angioplasty
with medical therapy for renal artery stenosis are
summarized in Table IV. The best known and most
widely quoted of these was the Dutch Renal Artery
Stenosis Intervention Cooperative (DRASTIC)
trial24; many of its features have generated contro-
versy. The categoric BP responses at 12 months are
often overlooked: the angioplasty group had more
improved (68% vs 38%), fewer worsened (9%
vs 33%; P=.002), and more normalized (7% vs
0%). Within the group originally assigned to drug
therapy, those who later underwent angioplasty
VOL. 10 NO. 7 JUly 2008
Table IV. Summary of Trials Comparing Angioplasty With Medical Therapy for Renal Artery Stenosis
First Author Plouin49
Intervention (No. Medical Rx: 26 (7 with
of patients) later angioplasty); 23
angioplasties (2 stents; 3
with later angioplasty)
Primary end Ambulatory BP after 6
point months
No differences in: Primary end point,
clinic BP measured by
oscillometric device
Significant Fewer BP medications and
differences in: physician-measured office
BP in angioplasty group
Abbreviations: BP, blood pressure; Rx, therapy.
Webster50
Medical Rx: 30 (5 with later
angioplasty); 21 angioplasties; 2
nephrectomies; 2 bypasses
Changes in BP and serum
creatinine at 6 months vs baseline
Primary end points, cardiovascular
outcomes (354 months)
Lower BP in those with bilateral
disease who received intervention;
40 complications after 135
angioplasties
Van Jaarsveld24
Medical Rx: 50 (22 with later
angioplasty); 56 angioplasties
(unsuccessful in 4; 2 with stent; 3 with
later surgery)
Office BP, serum creatinine, creatinine
clearance after 12 months
Primary end points
Fewer BP medications in angioplasty
group at 3 months; see text for further
discussion

Table V. Summary of 3 Ongoing Clinical Trials of Medical Therapy Angioplasty With Stent Placement in Patients With
Atherosclerotic Renal Artery Stenosis
STAR ASTRAL CORAL
No. of patients 140 7501000 1080
Inclusion criteria Ostial renal artery stenosis 50%, Renal artery suitable for angioplasty 80%99% renal artery stenosis, or
CrCl <80 mL/min/1.73 m2 stent placement; no prior 60%80% stenosis with 20 mm
revascularization procedure for Hg trans-stenotic gradient; systolic
atherosclerotic renovascular disease BP 155 mm Hg on 2 BP meds
Interventions Angioplasty + stent vs medical Rx Angioplasty stent vs medical Rx Angioplasty + stent vs medical Rx
alone alone alone
ACE inhibitors Only as a last resort, after Not recommended Highly recommended
and/or ARBs randomization postrandomization postrandomization
Primary 20% Reduction in CrCl Mean slope of 1/Scr vs time Composite of CV death, stroke,
end point MI, HF hospitalization, or ESRD
Secondary Acute complications, late BP, urinary protein excretion, Mortality, subgroup analyses, 1/Scr
end points complications, renal artery serious vascular events, ESRD, vs time, BP, renal artery patency,
occlusion, doubling of Scr, ESRD, angiography patency at 12 renal resistive index, quality of life,
BP, pulmonary edema; CV months cost-effectiveness
morbidity/mortality
Recruitment 1 Year (?) 6 Years 4 Years
period
Planned mean 2 Years 1 Year 2+ Years
follow-up
Abbreviations: ACE, angiotensin converting-enzyme; ARBs, angiotensin II receptor blockers; ASTRAL, Angioplasty and Stent for
Renal Artery Lesions; BP, blood pressure; CORAL, Cardiovascular Outcomes in Renal Atherosclerotic Lesions; CrCl, creatinine
clearance; CV, cardiovascular; ESRD, end-stage renal disease; HF, heart failure; MI, myocardial infarction; Rx, therapy; Scr, serum
creatinine; STAR, Stent for Atherosclerotic Ostial Stenosis of the Renal Artery Study.

had a significantly greater decrease in BP from 3
to 12 months than those who were maintained on
drug therapy alone (P<.0001), suggesting a prob-
lem with the intent-to-treat analysis. According to
expert radiologists who reviewed all angiograms
after randomization, 5 patients in each group
had stenosis <50% (and did not meet one of the
original inclusion criteria). Renal angiography
was repeated at 12 months in 91 of the original
106 patients; 23 of 48 (48%) in the angioplasty
group had restenosis 50%, compared with 35
of 43 (81%) in the drug treatment group (includ-
ing 4 occlusions); these restenosis rates are much
higher than seen in previous studies. A full 35%
of the patients had normal CS findings, which
had been reported to predict little BP response to
angioplasty; this may be the reason that baseline
CS results were not predictive in this cohort. Two
meta-analyses of these 3 trials of angioplasty com-
pared with medical therapy have come to slightly
different conclusions, despite considering the same
210 patients.47,48 In one, no significant differences

VOL. 10 NO. 7 JULY 2008 THE Journal of Clinical Hypertension 531

 were found in any end point (BP, medications,
or renal function).47 Patient-specific data were
available to Ives and associates,48 who reported a
slightly larger overall reduction in BP in the angio-
plasty group (6.3/3.3 mm Hg; P=.02/.03) vs drug
treatment. The change in serum creatinine values
was not quite significant (P=.06), but favored the
angioplasty group.
Three comparative randomized trials have
recently been launched in Holland, the United
Kingdom, and the United States (Table V). Each
of these has short-term end points (BP and renal
function), but will observe all patients for cardio-
vascular and renal events during several years of
follow-up. The hope is that these trials will have
few crossovers and other confounders so that a
more evidence-based recommendation can be
given about angioplasty plus stent placement, in
addition to intensive medical therapy, with identifi-
cation of independent predictors of the success and
failure of each strategy.
Conclusions
Although there are many unanswered questions
about renovascular hypertension, most authori-
ties agree that: 1) the absolute risk for the disease
can be estimated with reasonable accuracy, using
only clinical information, thereby sparing many
patients further evaluation; 2) patients with a very
high absolute risk of disease should proceed to
angiography if they are willing to undergo revas-
cularization; 3) a screening test should be done in
those with an intermediate absolute risk of disease,
and the choice of test may depend more on local
expertise and cost than on a comparison of pub-
lished performance characteristics; 4) angioplasty
should be offered to patients with FMD; and 5) the
question of whether intensive medical therapy
(including an ACE inhibitor or ARB) for athero-
sclerotic renovascular hypertension is improved by
angioplasty plus stent placement may be answered
by ongoing research.
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