Curr Cardiol Rep (2017) 19: 75
DOI 10.1007/s11886-017-0894-2
PERIPHERAL VASCULAR DISEASE (CJ COOPER AND R GUPTA, SECTION EDITORS)
Renal Artery Stenosis: New Findings from the CORAL Trial
Rajesh Gupta 1 & Salem Assiri 1 & Christopher J. Cooper 1
Published online: 27 July 2017
# Springer Science+Business Media, LLC 2017
Abstract
Purpose of Review The goal of this review is to summarize
recent advances in the field and highlight important new in-
sights from the Cardiovascular Outcomes in Renal
Atherosclerotic Lesions (CORAL) trial regarding the optimal
management of patients with renal artery stenosis (RAS).
Recent Findings The CORAL trial demonstrated that subjects
with RAS had similar outcomes whether randomized to opti-
mal medical therapy alone or optimal medical therapy plus
renal artery stenting. Subgroup analyses have failed to dem-
onstrate that baseline blood pressure or lesion gradients can
predict which subjects may have improved response after stent
intervention. Importantly, urine albumin to creatinine ratio
appears to different subjects that may benefit from stent inter-
vention versus subjects that are unlikely to achieve any bene-
fit. In addition, there was a trend toward increase benefit in
subjects with greater percent stenosis.
Summary Atherosclerotic RAS is a frequent finding and is
often seen in patients with resistant hypertension, congestive
heart failure, chronic kidney disease, and rarely those who
need renal replacement therapy. Risk factors for RAS overlap
with those of generalized atherosclerosis including hyperlip-
idemia, smoking, hypertension, and diabetes. Patients with
CAD or PVD frequently have co-existing RAS. The manage-
This article is part of the Topical Collection on Peripheral Vascular
Disease
* Rajesh Gupta
rajesh.gupta@utoledo.edu
1
University of Toledo Medical Center, 3000 Arlington Ave, MS#
1118, Toledo, OH 43614, USA
ment of RAS has been controversial for many years. The
CORAL trial provides important insights into the optimal
management of subjects with RAS.
Keywords Renal artery stenosis . CORAL . Stent .
Hypertension
Introduction
Atherosclerotic renal artery stenosis (RAS) is a manifestation
of atherosclerosis affecting the renal arteries, typically at the
ostium of the vessel. In some patients, it may lead to disturbed
intrarenal hemodynamics and subsequent sequelae including
hypertension and chronic kidney disease. The prevalence or
RAS can vary from 1 to 5% in unselected populations with
hypertension, and up to 15–40% in populations with other
manifestations of atherosclerosis, such as peripheral vascular
disease (PVD) and coronary artery disease (CAD) [1–4].
RAS is oftentimes found in patients with hypertension,
chronic kidney disease, congestive heart failure, and other
sequelae of hypertension, including myocardial infarction
and stroke. The Cardiovascular Outcomes in Renal
Atherosclerotic Lesions (CORAL) trial was the largest ran-
domized controlled trial of medical therapy alone versus med-
ical therapy plus stent intervention for subjects with RAS. The
CORAL trial was designed to overcome limitations of prior
RCTs in this field and provide definitive evidence regarding
the optimal treatment strategies for subjects with RAS and
hypertension or chronic kidney disease (CKD).
The goals of this review are to provide an overview of the
evidence base for the management of RAS and to summarize
the best practices for treating this condition.
75 Page 2 of 6
Background Clinical Trial Overview
In the 1990s, several uncontrolled studies showed that renal
artery angioplasty with or without stenting resulted in blood
pressure reductions [5, 6]. Subsequently, randomized con-
trolled trials were performed to assess medical therapy versus
percutaneous intervention for RAS. The Angioplasty and
Stenting for Renal Artery Lesions (ASTRAL) trial and the
Stent Placement and Blood Pressure and Lipid-Lowering for
the Prevention of Progression of Renal Dysfunction Caused
by Atherosclerotic Ostial Stenosis of the Renal Artery (STAR)
trial assessed the usefulness of renal artery stenting with re-
spect to kidney function and showed no significant difference
in this key measure [7, 8]. The DRASTIC trial also evaluated
the effect of renal artery angioplasty without stenting on kid-
ney function but was unable to demonstrate any significant
difference in the primary endpoints [7]. Some criticisms of
these trials included that they may have enrolled some indi-
viduals with non-significant RAS and they did not have core
lab to confirm the severity of RAS.
CORAL Study Overview
The purpose of the CORAL trial was to measure the useful-
ness of renal artery stenting for the prevention of major ad-
verse renal and cardiovascular events in subjects with RAS.
Previous trials had focused on blood pressure response or
measures of renal function, but the CORAL trial was the first
RCT in the field of RAS that was powered for important
clinical endpoints including mortality, myocardial infarction,
stroke, congestive heart failure, worsening renal failure, and
progression to renal replacement therapy [9••].
The CORAL trial screened 5322 subjects and enrolled 947
in the randomized controlled trial. Subjects were enrolled be-
tween 2005 and 2010. The study inclusion criteria included
evidence of severe RAS by angiography, duplex ultrasound,
CT, or MRI AND either HTN with systolic blood pressure of
155 mmHg or higher while on at least two anti-hypertensive
agents, OR CKD with which was defined as an estimated
glomerular filtration rate (GFR) of less than 60 ml/min/
1.73 m2 of body surface area, as calculated with the use of
the modified Modification of Diet in Renal Disease (MDRD)
formula. Most subjects (about 70%) were enrolled based on
angiography with about 25% enrolled based on non-invasive
imaging including duplex ultrasound, computed tomography
angiography (CTA), or MRA [9••]. Of note, for all entry im-
aging, a core lab review of each study was required.
The primary end points were death from cardiovascular or
renal causes, stroke, myocardial infarction, hospitalization for
congestive heart failure, progressive renal insufficiency, or
permanent renal replacement therapy. The rate of the primary
end point was similar between participants who underwent
Curr Cardiol Rep (2017) 19: 75
stenting and medical therapy versus medical therapy alone
(35.1 and 35.8%, respectfully, HR with stenting 0.94; 95%
CI, 0.76 to 1.17; p = 0.58) (Fig. 1) [9••].
Renal Artery Stenosis: Contrast with Other Forms
of Atherosclerosis
Importantly, although atherosclerosis is a diffuse process, the
particular manifestations and treatment response may differ
based on the specific aspects of the local organ or vascular
bed. For example, CAD may present symptomatically with
angina or acute coronary syndromes. Similarly, lower extrem-
ity PVD may present symptomatically with claudication or
critical limb ischemia. Extracranial cerebrovascular disease
is usually asymptomatic until it causes a stroke or TIA, and
the mechanism is typically by atheroembolization, rather than
stenosis leading to reduction in blood flow. In addition, the
treatment response and indications for interventional treat-
ment vary by each organ system and vascular bed.
RAS poses a number of difficulties for the clinician. First, it
is usually asymptomatic, except for hypertension which is both
a highly prevalent condition and usually asymptomatic.
Second, it often co-exists with other co-morbid conditions
which also lead to chronic kidney disease, especially hyperten-
sion and diabetes mellitus. Therefore, it becomes difficult to
“untangle” the role of RAS versus these other conditions in
the clinical situations such as worsening CKD. Third, it can
be difficult to accurately diagnose RAS by non-invasive means.
Vascular duplex ultrasound requires a highly skilled
Fig. 1 Kaplan-Meier curves for the primary endpoint in the CORAL trial
(a composite of death from cardiovascular or renal causes, stroke,
myocardial infarction, hospitalization for congestive heart failure,
progressive renal insufficiency, or the need for permanent renal
replacement therapy)
(From: Cooper CJ, et al., Copyright © 2014 Massachusetts Medical
Society. Reprinted with permission) [9••].
Curr Cardiol Rep (2017) 19: 75
sonographer, a well-prepared patient, and a knowledgeable
interpreting physician to perform accurately and varying
criteria have been used to define severe RAS [10]. Criteria that
may be used are sensitive (example systolic velocity >180 cm/
s), so as to detect RAS when it is present, or more specific
(example systolic velocity >300 cm/s), when an affirmative
diagnosis needs to be made. CTA and MRA both involve con-
trast agents with relative or absolute contraindications in sub-
jects with chronic kidney disease and both frequently overesti-
mate the severity of RAS. Fourth, the “gold standard” diagnos-
tic measurement, angiographic percent stenosis, has high levels
of interobserver variability and poor correlation with other
measures of stenosis severity such as pressure gradients [11].
Lastly, there is poor correlation between different diagnostic
modalities and “severe” RAS is difficult to define and identify
[12]. All of these problems pose difficulties for the interven-
tional treatment of RAS.
In addition to all of these difficulties, there are unique phys-
iological aspects of the kidneys. Relative to other organs, the
kidneys receive high blood flow due to their role in filtration
of the blood supply, yet oxygen extraction in the healthy kid-
ney is relatively low [13, 14].
The kidney has multiple mechanisms to maintain adequate
renal perfusion and oxygenation. The seminal work of
Goldblatt demonstrated that reduction in blood flow to the
kidney results in increased systemic blood pressure [15].
The tubuloglomerular feedback mechanism involves sensing
of sodium by the macula densa and subsequent release of
renin which leads to activation of the renin-angiotensin-
aldosterone system and increased blood flow to the kidneys
as well as systemic hypertension. In addition, the sympathetic
nervous system also regulates renal blood flow. RAS leading
to impairment of renal arterial blood flow results in activation
of the renin-angiotensin-aldosterone axis with sequelae that
include vasoconstriction, sodium and water retention, aldoste-
rone secretion, sympathetic nervous system activation, vascu-
lar remodeling, and hypertension. Interrupting this pathogenic
cascade provides the rationale for renal artery stenting; how-
ever, the reality is more complex.
Varying Response to Stent Intervention
Multiple studies have demonstrated a varying response to
stent intervention with some patients having improved renal
function, some unchanged, and some developing worsening
renal function after stent intervention. Post procedural renal
function deterioration has been reported to be as high as 20–
40%. Contrast nephropathy and atheroembolism may play a
role in this observed deterioration.
Attempts have been made to assess embolic protection in
stent intervention for RAS.
Page 3 of 6 75
Laird and Rocha-Singh used an embolic protection system
in patients undergoing angioplasty and stenting for atheroscle-
rotic RAS which showed feasibility, no clinical evidence of
peripheral atheroembolism, favorable trends in blood pressure
control in 6-month follow-up, and no temporary or permanent
renal replacement therapy [16].
Cooper et al. studied renal artery stenting and the role of
platelet inhibition with abciximab (Reopro, GP IIb/IIIa inhib-
itor) and embolic filter protection using the Angioguard de-
vice (Cordis) [17]. The trial was a 2 × 2 factorial design study-
ing the use of abciximab and the Angioguard filter during
renal artery stenting in 100 patients. Surprisingly, abciximab
alone and the Angioguard filter alone were not different than
the negative control (neither abciximab nor Angioguard fil-
ter), however, the group that received both abciximab and the
Angioguard filter did have an improvement [17].
It appears that renal artery stenting significantly activates
platelets and may also be associated with significant
atheroembolization. Other investigators have also assessed
various embolic protection devices and mechanisms and some
have documented significant atheroembolic debris during re-
nal artery stenting. The situation in the renal arteries may be
more similar to that of carotid artery stenting or stenting of a
saphenous vein bypass graft, which are both situations where
embolic protection has been demonstrated to be beneficial.
Certain locations of atherosclerotic plaque are more vulnera-
ble to atheroembolic injury, either due to the nature of the
atherosclerotic plaque or due to the unique nature of the vas-
cular beds in those organ systems. With regard to RAS, it
remains unknown if embolic filter protection is beneficial
since no properly powered trial has compared stent interven-
tion alone to stent intervention with embolic protection. The
role of embolic protection remains uncertain and it seems
unlikely that an adequately powered clinical trial will be per-
formed to answer this question.
What Constitutes Optimal Medical Therapy?
The CORAL trial represents the best standard for optimal
medical therapy in subjects with RAS. In the CORAL trial,
all subjects were treated with aspirin, a long-acting angioten-
sin receptor blocker (candesartan), a long-acting calcium
channel antagonist (amlodipine), and a statin, (atorvastatin.)
Hydrochlorothiazide was added if additional blood pressure
control was needed. This combination of anti-platelet therapy,
cholesterol lowering with a potent statin, and effective anti-
hypertensive medical therapy constitutes a robust medical in-
tervention for subjects with RAS.
With regard to the choice of the angiotensin II receptor
blocker (ARB), there are some basic science findings indicat-
ing unique efficacy with candesartan [18, 19], and although
this drug was not compared with ACE-I or other ARB, it was
75 Page 4 of 6 Curr Cardiol Rep (2017) 19: 75

well tolerated in the CORAL population. Importantly, ACE-I
or ARB medical therapy is often withheld in subjects with
RAS due to fears of worsening renal function. However, in
the CORAL trial, candesartan was well tolerated. Given the
importance of ACE-I/ARB therapy in the prevention of pro-
gressive CKD, subjects with RAS should be treated with
ACE-I or ARB (again, we favor candesartan since it is the
best studied ACE-I or ARB in subjects with RAS).
Physicians can closely monitor renal function after initiating
candesartan and a 25% rise in creatinine is acceptable, as long
as the level then stabilizes.
Insights from CORAL Subgroup Analyses
Murphy et al., in a post hoc subgroup analysis from the
CORAL study, found baseline blood pressure did not predict
response to stent intervention [20••]. This is an important ob-
servation since multiple investigators have shown that high
baseline blood pressure is associated with a greater reduction
in blood pressure after revascularization. Now, we understand
this likely represents regression to the mean. Furthermore,
there was no correlation between peak systolic pressure gra-
dient and response to either therapy arms in the CORAL trial.
Pressure gradients have been postulated as a means to confirm
“true severe” stenosis, but the utility of this metric to predict
response to stent intervention was not confirmed in the
CORAL trial. However, the number of subjects (199) that
had this measurement performed was modest.
There was a trend favoring stenting versus medical therapy
with the highest category for stenosis severity (stenosis
>77.05% measured by core lab), but this was not statistically
significant (p = 0.25) (Fig. 2). These subgroup analyses may
be underpowered and it remains possible that subjects with
severe stenosis may benefit from stent intervention, but this
subgroup made up only 25% of the CORAL cohort and rep-
resents a small subset of the total population of patients with
RAS. Lastly, it may be difficult to identify these patients in the
real world given discrepancies between core lab and operator
classification of percent stenosis and failure of pressure gradi-
ent to provide meaningful discrimination between responders
and non-responders to stent intervention. It remains to be

Fig. 2 Baseline percent stenosis

and freedom from the primary
composite end point through
5 years in in the CORAL trial. a
Core lab percent stenosis divided
into quartiles (<60.22, 60.22 to
<68.46, 68.46 to <77.05,
≥77.05%). Log-rank test between
groups for first quartile
(<60.22) = 0.4895. Log-rank test
between groups for second
quartile = 0.4780. Log-rank test
between groups for third
quartile = 0.3065. Log-rank test
between groups for fourth
quartile = 0.1487. The p value is
for all available follow-up (not
limited to 5 years). b Core lab
percent stenosis divided into
clinically significant categories
(<60, 60 to <80, ≥80%). Log-rank
test between groups for the first
category (<60) = 0.3992. Log-
rank test between groups for
second category = 0.1023. Log-
rank test between groups for the
third category = 0.2487. The p
value is for all available follow-up
(not limited to 5 years).
(Reprinted from Murphy TP
et al., Copyright © 2015, with
permission from Elsevier) [20••]
Curr Cardiol Rep (2017) 19: 75
Fig. 3 Freedom from the primary
composite end point through
5 years of follow-up by treatment
group and urine albumin/
creatinine ratio (uACR).
(Reprinted from: Murphy TP
et al., Copyright © 2016, with
permission from Wolters Kluwer)
[21••]
determined if additional measurements such as IVUS imag-
ing, measures of renal perfusion, biomarkers, or measures of
organ function can discriminate between responders and non-
responders to stent intervention.
Murphy et al. also performed a post hoc analysis of the
CORAL trial data based on urine albumin/creatinine ratio
(UACR) [21••]. The cutoff value for UACR was 22.5 mg/g
based on the median value for this measurement. Subjects
with lower than median UACR had fewer clinical events with
renal artery stent treatment than those assigned to medical
treatment (Fig. 3). However, subjects with higher than median
UACR did not demonstrate these benefits.
Urine albumin to creatinine ratio provides a simple mea-
surement of organ function, and importantly, addresses one of
the main “competing risks” for RAS interventions, namely,
intrinsic renal diseases including hypertensive and diabetic
nephropathies. The hypothesis is that patients with RAS and
healthy kidneys may benefit from renal artery stent interven-
tion. Subjects with poor organ function, measured as an ele-
vated UACR, may not benefit. Further studies are needed to
investigate this observation from the CORAL trial.
Conclusion
RAS is a common condition in subjects with advanced ath-
erosclerosis. Insights from the CORAL trial have demonstrat-
ed that for most subjects with RAS, optimal medical therapy is
the best treatment strategy.
Subgroup analysis from the CORAL trial has failed to iden-
tify conventional baseline markers, such as blood pressure se-
verity, as good predictors of response to stent intervention. The
one baseline variable that appears promising for predicting a
favorable response to stent intervention is the urine albumin to
creatinine ratio, with a low UACR portending a favorable
response.
Page 5 of 6 75
The CORAL data did not identify baseline hypertension
severity, peak systolic pressure gradient across the stenosis,
or angiographic stenosis severity as predictors of response to
stent intervention. It is possible that subjects with severe ste-
nosis and subjects with low urine albumin to creatinine ratio
may benefit from stent intervention, but this may be a very
small subgroup of RAS patients. The role of embolic protec-
tion and potent anti-platelet therapies remains to be
determined.
All patients with RAS should be treated with optimal med-
ical therapy consisting of anti-platelet therapy, high-intensity
statin medical therapy, and effective anti-hypertensive treat-
ments with long-acting drugs that may include amlodipine,
candesartan, and the addition of a thiazide-type diuretic if
needed to achieve goal blood pressure.
Compliance with Ethical Standards
Conflict of Interest Rajesh Gupta and Salem Assiri declare that they
have no conflict of interest.
Christopher J. Cooper reports grants from NIH and Pfizer, grants and
other from AstraZeneca, and grants and other from Cordis.
Human and Animal Rights and Informed Consent This article does
not contain any studies with human or animal subjects performed by any
of the authors.
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