The document discusses renal artery stenosis, including its anatomy, causes, diagnosis and treatment. Renal artery stenosis is the leading cause of secondary hypertension and can lead to resistant hypertension, declining renal function and cardiac issues. It is most commonly caused by atherosclerosis (90%) or fibromuscular dysplasia (10%). Diagnosis involves tests like renal artery duplex imaging, CT angiography and MRA. Treatment involves optimal medical management as well as catheter-based interventions like renal artery stenting for significant atherosclerotic lesions, while angioplasty with possible stenting is recommended for fibromuscular dysplasia lesions. Surgery is also an option in some complex cases.

1. RENAL ARTERY STENOSIS
DR NAJEEB U SOFI
LPS INSTITUTE OF CARDIOLOGY

2. NORMAL RENAL ARTERIAL ANATOMY
 Originate from the lateral sides of the aorta at the level of the
superior border of the second lumbar vertebra directed slightly
anteriorly usually 1-2 cm below the superior mesenteric artery origin.
 The right RA originates from the anterolateral aspect of the aorta and
immediately turns posteriorly to course beneath the inferior vena
cava.
 The left RA originate from the posterolateral surface of the aorta and
courses posteriorly the surface of the aorta and over the psoas
muscle.

3.  Renal artery stenosis is the leading cause of secondary
hypertension and may lead to :
1. Resistant (refractory) hypertension,
2. Progressive decline in renal function, and
3. Cardiac destabilization syndromes (Flash pulmonary edema,
recurrent heart failure, or acute coronary syndromes)

4. RENAL ARTERY STENOSIS
 Atherosclerotic (90%)
 Fibromuscular dysplasia (10%)
 Aortorenal dissection
 Vasculitis involving the renal artery (i.e. PAN)
 AVMs involving the renal artery
 Irradiation of the renal artery
 Neurofibromatosis
 Scleroderma

5. ATHEROSCLEROTIC RAS
• Patient 6th decade or older.
• More often male
• Associated with diseased aorta
• Typically involves the ostium
and/or proximal one-third of
the renal
• Can be unilateral or bilateral
• 70-80% have unilateral
disease

6. FIBROMUSCULAR DYSPLASIA
 Young patients –more commonly females.
 Commonly asymptomatic
 Prevalence 2-6 %
 Renal artery involvement is seen in 60% of cases
 >60% of patients have bilateral disease.
 Medial fibroplasia (90%)>> Intimal (10%) or adventitial
 Location: distal two-thirds of main renal artery, in 25%, disease extends into
segmental arteries
 Right renal artery is affected more frequently
 Progressive renal stenosis is seen in 37% of cases and loss of renal mass in 63%.
 Other arteries can also be involved (carotid, vertebral, iliac, and mesenteric). All
patients need head imaging to r/o cerebral aneurysms

7. ABDOMINAL AORTOGRAM REVEALED A LEFT RENAL ARTERY FIBROMUSCULAR DYSPLASIA WITH THE
TYPICAL “STRING OF BEADS” APPEARANCE

8. PREVALENCE OF ATHEROSCLEROTIC RAS
 M.C secondary cause of of HTN 2-5 %
 General population 0.1%
 Hypertensives 1-4%
 Aged 65 years and older 6.8%
 Diabetics 8%
 Malignant HTN 20 - 30%
 Malignant HTN & renal insufficiency 30 - 40%
– 6.8% in healthy adults > 65 years old
– Evaluation with renal artery duplex of 834 patients consecutive patients who
were participants in the Forsyth county cohort of the Cardiovascular Health Study
(J Vasc Surg. 2002;36:443–51).

9. RAS IS COMMON IN PATIENTS
WITH VASCULAR DISEASE
 Prevalence of RAS
 Proven MI 12%
 Undergoing cardiac catheterization 6-19%
 Lower extremity PVD 22-59%
 Predictors of RAS in patients undergoing cardiac
catheterization
 CAD; Age; PVD; serum creatinine; hypertension

10.  3 year mortality
 26% in patients treated with stents (Circulation 1998;98:642-
647)
 28% in patients managed medically (Mayo Clin Proc
2000;75:437)
 4 year mortality
 43% in patients with RAS discovered incidentally at cardiac
catheterization (Kidney International 2001;60:1490-1497)
 35% in patients with RAS discovered incidentally at cardiac
catheterization (JASN 1998;9:252-256)
 26% in a multi-center study of patients undergoing
percutaneous renal revascularization (Circulation
1998;98:642-647)
 5 year mortality
 33% in a single-center study of patients undergoing
percutaneous renal artery revascularization (Catheter
Cardiovasc Interv. 2007;69:1037)

11. CLINICAL POINTERS: PROGRESSION OF
ATHEROSCLEROTIC RAS
 48% of patients with <60% stenosis progress to
>60% over 3 years
 39% patients with >75% stenosis progress to
complete occlusion over 3 years
 Average progression ~7% per year
 Progression of RAS and loss of renal function occur
independently of blood pressure control
D. Lao et al.

12. PROGRESSION OF RENOVASCULAR DISEASE
RESULTS IN RENAL ATROPHY
 204 kidneys in 122 patients with RAS
 6 monthly serial duplex scanning
 Defined as > 1cm reduction in length
2 year incidence of renal atrophy:
Normal RA 5.5%
< 60 % stenosis 11.7%
> 60 % stenosis 20.8%
Risk of atrophy increased by systolic hypertension
(> 180mm Hg) and a high peak systolic velocity
Caps et al, Kidney International, 1998

13. CLINICAL MANIFESTATIONS
Renal Artery
Stenosis
Renovascular
HTN
Ischemic
Nephropathy
Cardaic
Destablization
Syndromes
Incidental
RAS

14.  Unilateral RAS results in vasoconstrictor-mediated HTN, while
bilateral or solitary kidney RAS results in HTN with volume overload.
 CARDIAC DESTABILIZATION SYNDROMES. Uncontrolled HTN
and volume retention associated with ARAS play an important role in
the destabilization of patients with ACS or CHF.
 The Pickering syndrome, sudden onset, “flash,” pulmonary edema,
is a commonly recognized destabilization syndrome resulting from
ARAS. The presence of these syndromes should prompt an
investigation for RAS.
 ISCHEMIC NEPHROPATHY. If the cause of CKD is ischemic nephropathy,
this is potentially reversible. Some studies suggest that as many as 12% of
patients with end-stage renal disease have CKD attributable to progressive
ischemic nephropathy from ARAS. Atrophy of the kidney occurs as a
consequence of the progression of ARAS . In patients with CKD and severe
ARAS, renal artery stenting is most beneficial in those with a more rapid
rate of decline.

15. Advanced nephropathy that is not likely to benefit
from revascularization has been described by
1. Proteinuria >1 g/day,
2. Kidney pole-to-pole length of <7 cm, or
3. Hemodialysis for >3 months

16. WHO SHOULD WE SCREEN?

17. CLUE
 Onset of hypertension <age 30 years
 Onset of severe hypertension after the age of 55 years
 Malignant or refractory hypertension
 Unexplained renal atrophy or size discrepancy of >1.5
cm between kidneys
 Worsening renal function upon initiation of ACE-I/ARB
therapy
 Sudden, unexplained pulmonary edema (especially in
azotemic patients).
 Unexplained progressive renal insufficiency
 Presence of multivessel coronary artery disease or
peripheral arterial disease
 Unexplained congestive heart failure or refractory
angina
 Abdominal bruit (more than 75% of patients)

19. DIAGNOSTIC TEST (CURRENTLY RECOMMENDED)
1. Renal artery duplex imaging
2. Computed tomography
3. Magnetic resonance angiography
4. Conventional Angiography

20. NONINVASIVE DIAGNOSTIC MODALITIES
RENAL ARTERY ULTRASOUND
 Safe, inexpensive and widely available,
 Images of the renal arteries as well as blood flow velocity and
pressure waveforms,
 Information regarding kidney size and renal resistive index
 Body habitus dependent
 Operator dependent
 May miss accessory arteries
 Allows post intervention surveillance

21.  Renal artery/aortic Peak Systolic velocity ratio >3.5
(Sn 84%, Sp 92%) for 60% stenosis
 Renal artery Peak Systolic Velocity (PSV) >200 cm/s (Sn and
Sp ~98%) for > 50% stenosis.
 End Diastolic Velocity (EDV) >150 cm/s (RAS >80%)
 Significant discrepancy in kidney size
 Acceleration time: (time period between the onset of systolic
upstroke and the initial peak velocity (compliance peak)). Normal
<100 ms (usually 40–50 ms)→ if >100 ms associated with RAS
60%
 Renal resistive index (RRI = 1 − EDV/PSV):
(Normal < 0.7, nephrosclerosis > 0.7)

22. DUPLEX ASSESSMENT OF RAS
Duplex Criteria Stenosis
RAR<3.5 and
PSV<200 cm/sec
0-59%
RAR >3.5 and
PSV>200 cm/sec
60-99%
RAR>3.5 and
EDV > 150 cm/sec
80-99%
Absence of flow and low
amplitude parenchymal signal
Occluded

23.  The renal resistive index (RI) is a commonly used measure of
resistance to arterial flow within the renal vascular bed.
 An elevated RI is considered to be an indicator of
nephrosclerosis and intrinsic kidney disease
 Despite initial studies suggesting lack of benefit of RAS
therapy with RRI >0.8,
 More recent studies suggest that a significant response in
renal function may be obtained despite an abnormal resistive
index, but this response is more blunted.
 Therefore, RRI should not use as the sole decision maker to
revascularize or not.

24. PREDICTING OUTCOMES OF THE REVASCULARIZATION
 Resistive Index:
 1-end-diastolic velocity/peak systolic velocity
 6000 Patients with HTN/ and clinical suspicion, screened
for RVH.,
 131 had RAS, .
 Patients with resistive index >0.8
 80% had decline in renal function
 50% dialysis dependant
 Only 1 patient had > 10mmhg reduction in BP.
 Patients with RI < 0.8
 94 % had significant reduction in BP.
 3% had decline in renal function
Radermacher, J, et al. Use of Doppler ultrasonography to predict the outcome of therapy
for renal-artery stenosis. N Engl J Med 2001; 344:410.

25. OUTCOMES PREDICTED BY RRI
 Radermacher et al NEJM. 2001;344:2244-49

26. COMPUTED TOMOGRAPHY ANGIOGRAPHY
 Excellent images can be obtained
 Sensitivity >91%; Specificity 85–99%
 Image interpretation may be difficult in heavily
calcified arteries;
 Involves the use of ionizing radiation and iodinated
contrast

27. MAGNETIC RESONANCE ANGIOGRAPHY
 Identifies accessory renal arteries
 Provides additional anatomical
information
 No radiation
 No nephrotoxic contrast
 Sensitivity 90–100%; Specificity 76–
94%
 MRA is preferred in heavily calcified
arteries, which can be a greater
challenge for CTA.
 Looses accuracy in distal segments
(FMD)
 Gadolinium-based contrast associated
with nephrogenic systemic fibrosis in
patients with moderate-to-endstage
renal failure;

29. INVASIVE STENOSIS ASSESMENT
 An angiographic ARAS >70% diameter stenosis is severe or
significant, and diameter stenoses of 50% to 70% are considered
moderately severe, of uncertain hemodynamic significance.
 For moderately severe stenoses, confirmation of the hemodynamic
severity of the RAS is recommended prior to stenting .
 A resting or hyperemic translesional systolic gradient of >20 mm Hg,
a resting or hyperemic mean translesional gradient of >10 mm Hg, or
a renal fractional flow reserve (RFFR) <0.8 will confirm
hemodynamically severe ARAS .
 The translesional pressure gradient should be measured using a
nonobstructive catheter or a 0.014-inch pressure wire. Hyperemia
may be induced with an intrarenal bolus of papaverine at a dose of
40 mg or an intrarenal bolus of 50 mg/kg dopamine

31. OPTIMAL MEDICAL TREATMENT
 Antihypertensive
 LDL to goal
– Currently <100 (or 70) mg/dl
 Diabetes Management
– HbA1c to target (<7%)
 Smoking Cessation
 Anti-platelet therapy (aspirin +/-
clopidogrel)

32. •
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
• ACE inhibitors are effective medications for
treatment of hypertension associated with RAS.
• Calcium-channel blockers are effective
medications for treatment of hypertension
associated with unilateral RAS.
• Beta-blockers are effective medications for
treatment of hypertension associated with RAS.
Pharmacological Treatment of
Renal Artery Stenosis
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII • Angiotensin receptor blockers are effective
medications for treatment of hypertension
associated with unilateral RAS.
ACC/AHA Guidelines
ACC/AHA Guidelines

33. CATHETER- BASED INTERVENTIONS FOR RAS
 Renal stent placement is indicated for
ostial atheroesclerosic RAS lesions that
meet the clinical crietria for intervention.
 Balloon angioplasty with “bail-out” stent
placement if necessary is recommended
for fibromuscular dysplasia lesions.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
ACC/AHA Guidelines
ACC/AHA Guidelines

34. SURGERY FOR RENAL ARTERY STENOSIS
 Atherosclerotic RAS in combination with pararenal
aortic reconstructions (in treatment of aortic
aneurysms or severe aortoiliac occlusive diseease.
 Fibromuscular dysplastic RAS with clinical indications,
especially those exhibiting complex disease that extends
into the segmental arteries and those having
macroaneurysms.
 Atheroeclerotic RAS and clinical indications for
intervention, especially those with multiple small renal
arteries or early primary branching of the main renal
artery.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
ACC/AHA Guidelines
ACC/AHA Guidelines

36. RENAL ARTERY STENTING
Effect and Indication

37. GOAL OF RENAL STENTING
Clinical goals
 Improve control of hypertension
 Preserve or restore renal function
 Treat other potential adverse physiologic effects of
severe renal artery stenosis (congestive heart
failure, recurrent flash pulmonary edema, and
angina)

38.  ARAS is often due to bulky aorto-ostial plaque,
balloon angioplasty alone is frequently ineffective
because of the recoil associated with these bulky
plaques, making renal artery stenting the preferred
method of treatment.

39. MINIMIZING COMPLICATIONS
 The complication rate approaches 2%.
 The most common complications related to femoral
access (hematoma, pseudoaneurysm,
arteriovenous fistula),
I. Atheroembolism,
II. Retroperitoneal hematoma,
III. Renal artery rupture,
IV. Aortic and renal artery dissection,
V. Contrast nephropathy,
VI. Renal infarction, and
VII. Death

40.  Technical issues one should consider in order to
reduce complications include
I. Radial artery vascular access,
II. Embolic protection devices (EPDs),
III. Catheter-in-catheter technique,
IV. No-touch technique,
V. Stent sizing with intravascular ultrasound (IVUS),
VI. Hydration before and after angiography is
performed

41. NO-TOUCH TECHNIQUE
 0.035-inch, J-tip
guidewire is advanced
in the abdominal aorta
superior to the renal
arteries.
 Over this wire, the
guide catheter is
advanced in proximity
to the renal artery

42.  0.035 inch wire is then
retracted to the soft
portion of the wire
 So that the guide
catheter begins to
assume its shape and
approach the ostium of
the renal artery.
 The J-shaped portion
of the wire is left
outside to guide
against the aortic wall

43.  Guiding catheter is
gently rotated and
aligned with the renal
ostium,
 With the J wire
preventing guiding
catheter intubation into
the renal artery.
 From this position, a
0.014-inch wire is
advanced through the
guide and into the
distal renal artery

44.  0.035-inch J wire is
then removed, and
 Guiding is advanced
over the 0.014 inch
wire to engage the
renal artery.

45. NO TOUCH”” TECHNIIQUE

46.  Most renal ostial lesions originate from the aortic
atherosclerosis.
 Flank pain should be closely monitored because it
indicates stretching of the adventitia.
 If detected, higher-pressure inflations should be avoided
 It is critically important to avoid over dilation as aorta or
renal artery dissection is a dreaded consequence
 The size of the balloon-mounted stent should be sized
according to the normal renal caliber and not the
adjacent post stenotic dilatation that is often present
distal to a hemodynamically significant stenosis.

47.  Post balloon angioplasty angiogram is performed to
document the procedural result.
 Radiographic evidence of either residual stenosis or
renal artery dissection constitutes suboptimal
angioplasty results, which warrants an immediate renal
artery stent placement.
 Atherosclerotic involvement of the renal artery usually
involves the vessel orifice, which typically requires a
balloon-expandable stent placement.
 Most atherosclerotic renal artery lesions demonstrate
significant recoil after balloon angioplasty and therefore
require stent placement
 Stent is deployed by expanding the angioplasty balloon
to its designated inflation pressure, which is typically
less than 8 atm

48.  For ostial lesions, it is important to deploy the stent
with the proximal segment protruding 1–2 mm
inside the aorta and to
 Flare the extending portion with a compliant balloon
 Efficacy of drug-eluting stents (DES) is unknown
 Use of DES in the initial treatment does not
recommended at this time.
 For in-stent restenosis, DES can be considered
depending on the size of the renal artery.

49.  Completion angiogram should be done to assess
proper coverage of the renal ostium by the stent,
the main renal artery, and its branches for signs of
dissection or spasm and the renal parenchymal
blush to exclude evidence of atheroembolization.

52. FOLLOW UP AND SCREENING AFTER RAS STENTING
 Dual antiplatelet therapy with aspirin (325 or 162
mg daily) and clopidogrel (75 mg daily) for at least
30 days;
 Then monotherapy with aspirin (81 mg daily)
chronically.
 Surveillance is not standardized.
 Renal ultrasound to be performed within 1–2 weeks
after RAS stenting to establish a new baseline,
 Followed by US in 6- and 12-months.
 CT and MRI are less useful given the artifact seen
in the presence of the stent.
 Regular monitoring of blood pressure and renal
function.

53.  Technical success:98-100%
 Long term patency rate 80%-95%
 Complications:
 Mortality 1-3%
 Major complications: 3-5%
 Minor complications 10-20%

54. COMPLICATIONS
 Most complications are related to arterial access.
 Include groin hematomas, retroperitoneal
hemorrhage, pseudoaneurysm, arteriovenous
fistula, and infection.
 Atheroembolism into the renal or peripheral
vascular bed : cholesterol embolization
 Dissection of renal artery or the wall of the aorta
 Acute or delayed thrombosis
 Rupture of renal artery
 Renal perforation

55. RENAL ARTERY EMBOLIZATION
A, Baseline selective renal
angiogram showing tight
ostial stenosis with normal
filling of the renal arteries to
the cortex
B, Poststent angiogram with
poor filling of the distal renal
arteries caused by
embolization

56. ARTERIOGRAM DEMONSTRATING RENAL ARTERY RUPTURE AND
EXTRAVASATION OF CONTRAST AFTER BALLOON ANGIOPLASTY

59. EFFECT ON RENAL FUNCTION
Lim and Rosenfield, Curr Int Cardiol 2000,2:130-139.

60. RESULTS OF REVASCULARIZATION FOR ISCHEMIC
NEPHROPATHY
 33 patients with bilateral RAS or RAS in solitary
kidney.
 Follow up: 20±11 months.
 Significant improvement in 72%; mild improvement
in 28%.
 Preservation of renal size in all patients.
 Watson et al. Circulation 2000

61. SIGNS THAT A PATIENT WITH ISCHEMIC
NEPHROPATHY WILL BENEFIT FROM
REVASCULARIZATION
 Normal distal arterioles.
 Bilateral disease.
 Recent onset of renal insufficiency.
 Resistive Index (Doppler sonography) <80
 Extremely limited renal function (cr>2.5 mg/dl)
 Uder M, Huke U CVIR 2005

62. CLINICAL OUTCOME OF RENAL ARTERY STENT
PLACEMENT

63. EFFECT ON HYPERTENSION

64. WHY RENAL FUNCTION MAY DETERIORATE
AFTER REVASCULARIZATION
 Contrast nephropathy.
 Cholesterol embolization.
 Exposure of diseased glomeruli to high blood
pressure.

65. ASTRAL STUDY
 806 patients were randomized to either medical
therapy alone (403 patients) or medical therapy and
revascularization, PTA and/or stent (403 patients)
 The authors concluded that stenting is not superior
to medical therapy.
 This study has been criticized because of a lot of
limitations,

66.  Patients were excluded if their physicians thought that
they might not benefit from intervention.
 40% of patients had a stenosis <70% unlikely to be
hemodynamically significant
 Pressure gradient was never measured in any patient.
 Some patients had a renal length of 6 cm, which is
generally considered as a contraindication for a
revascularization
 40% of the stented groups were unlikely to have
benefited even from a successful intervention without
complications, since they probably did not have the
disease ‘‘ischemic nephropathy’’ in the first place
 Higher complication rate and inexperienced operator

67. CORAL TRIAL
 It was a larger trial of 947 participants having
hypertension and RAS >80% or more than 60% with a
pressure gradient of 20 mmHg.
 It compared renal artery stenting with medical therapy
versus medical therapy alone.
 Optimal medical therapy was given in both groups.
 The primary endpoints were major cardiovascular or
renal events (cardiovascular or renal death, MI, CHF,
stroke, progressive renal insufficiency and need of renal
replacement therapy).
 Secondary endpoints were all cause mortality and
individual components of primary endpoint.
 The authors of the trial concluded that there was no
difference in the cardiovascular and renal events or all
cause mortality seen in the two groups.

68.  CORAL although more robust in its patient
selection,
 Still included patients with stable disease and has
similarly been criticised as proving only that treating
non-significant lesions does not significantly change
outcomes
 The mean % stenosis: (67.3±114%)
 The mean blood pressure: 149.9±23.2 mmHg

70.  The CORAL trial as well as the ASTRAL trial demonstrated
that in patients with moderate ARAS (50% to 70% diameter
stenosis) and unconfirmed hemodynamic severity of RAS and
HTN, there was no benefit of revascularization over GDMT
alone.
 In a meta-analysis of 678 patients, the renal artery stenting
procedure
1. Success rate was 98%,
2. Clinical improvement in HTN was only about 70%, and
3. Improvement in renal function occurred in 30% of patients,
with stabilization in 38%

71. RATIONALE FOR RENAL ANGIOPLASTY
STENTING PATIENT SELECTION
 For good result after renal angioplasty stenting
Good patient/lesion selection is mandatory before
deciding which treatment to propose
 Peak systolic gradient ≥20 mmHg or a mean
pressure gradient of 10 mmHg considered as
hemodynamically significant
 Mean gradient > 20 mmHg after Dopamine is highly
predictive of blood pressure improvement.
 A ratio of aortic pressure/poststenotic pressure
<0.90 is highly predictive of renovascular
hypertension and blood pressure improvement.

72.  Intravascular ultrasound, fractional flow reserve can
also help to determine the severity of the stenosis
 Biomarkers: Renin, Brain Natriuretic Peptides.
 A ratio between the two kidneys, or the renal vein
renin ratio (RVRR), of greater than 1.5 is indicative
of functionally important renovascular hypertension,
and it also predicts a favorable response from
renovascular hypertension.

73. FAVORABLE PREDICTORS
SUCCESSFUL OUTCOME FOR CONTROL OF
HYPERTENSION
 Rapid acceleration of hypertension over the prior
weeks or months
 Presence of “malignant” hypertension
 Hypertension in association with flash pulmonary
edema
 Contemporaneous rise in serum creatinine
 Development of azotemia in response to ACE
inhibitors administered for control of hypertension.

74. FAVORABLE PREDICTORS
SUCCESSFUL SALVAGE OR PRESERVATION OF
RENAL FUNCTION
 Recent rapid rise in creatinine, unexplained by
other factors
 Azotemia resulting from ACE inhibitors
 Absence of diabetes or other cause of intrinsic
kidney disease
 Presence of global renal ischemia, wherein the
entire functioning renal mass is subtended by
bilateral critically narrowed renal arteries or a
vessel supplying a solitary kidney.

75. UNFAVORABLE PREDICTORS
 Renal atrophy demonstrated by kidney length <7.5
cm on ultrasound
 High renal resistance index detected by duplex
ultrasound
 Proteinuria > 1gm/day
 Hyperuricemia
 Creatinine clearance <40 mL/minute

76. CONCLUSIONS
 With modern equipment and skilled operators, renal
artery stenting can be performed with high technical
success (>98%) and low restenosis (15-20%)
 Incidental RAS is not an indication for
revascularization.
 Following successful renal stenting there is slowing
of deterioration of renal function and prevention of
renal atrophy

77. CONCLUSIONS
 HTN is rarely cured (<10%-15%) in patients with
atherosclerotic RAS
 The majority (>50%) will have some benefit with
regards to HTN control and/or decreased anti-
hypertensive drugs following renal stenting
 Revascularization is indicated in hypertensive
patients with RAS if renal mass loss or renal
function decline is observed during hypertensive
treatment.

79. THANK YOU