Ischemic nephropathy (IN), also known as azotemic renovascular disease, is impairment of renal function caused by reduced blood flow to the kidneys beyond occlusive disease of the main renal arteries. The most common causes are atherosclerotic renal vascular disease (ASRVD) and fibromuscular dysplasia (FMD). IN is more prevalent with increasing age and can lead to end-stage renal disease in 12% of cases. Clinical features that suggest IN include treatment-resistant hypertension and worsening renal function. Diagnosis involves Doppler ultrasound or angiography. Treatment aims to control blood pressure and protect renal function through medication, angioplasty, stenting or surgery depending on the

1. Ischemic nephropathy
Presenter : DR. Kushal. D. P

2. Synonyms
• “Azotemic renovascular disease” or or ischemic renal disease
(IRD)

3. Definition
• The term “ischemic nephropathy” (IN) means impairment of
renal function beyond occlusive disease of the main renal
arteries
• Azotemic renovascular disease” is other term coined by
some authors suggesting that loss of renal viability may not
directly be associated with impairment in oxygenation of
renal tissue as less than 10% of the blood is needed to fulfill
the metabolic requirement

4. • Renovascular hypertension is defined as a syndrome of
elevated BP (systolic and/or diastolic) produced by any
condition that interferes with arterial circulation to the
kidneys.
• Of the conditions that may produce the syndrome of RVH,
main vessel RA stenosis is by far the most common. The two
major causes of main renal artery disease are fibromuscular
dysplasia (FMD) and atherosclerotic renal vascular disease
(ASRVD).

5. Epidemiology
• Mean age of patients with IN to be 68.7 years of which
97.4% were hypertensive, 69.8% smokers and 62.95% having
hypercholesterolemia, evidences of atherosclerosis at other
vascular beds in 82% of these patients, 65% showing
peripheral arteriopathy.
• The prevalence of IN has been found to be increasing with
age and was found to be responsible for 5%-22% cases of
renal dysfunction in patients above 50 years. 12%
progressing to ESRD with an average decline in GFR of 8
mL/min

6. • In patients undergoing angiography of the peripheral or
coronary circulation, ASRVD is found in 11% to 42%.
• One population-based study of 870 patients older than 65
screened with RA duplex ultrasound found a 6.8%
prevalence of ASRVD, defined as greater than 60% stenosis.
• Autopsy series report an overall prevalence of 4% to 20%,
with progressively higher rates for those older than 60 years
(25% to 30%) and 75 years (40% to 60%).

7. • RA stenosis from ASRVD contributes to the decline in renal
function in 15% to 22% of patients reaching ESRD.
• The prevalence of clinically apparent renovascular FMD is
estimated at 4 in 1000, with a lower prevalence of
cerebrovascular involvement of 1 in 1000.
• Screening angiography in potential kidney donors suggest that
FMD observed in 3% to 6% of individuals.
• FMD has a female predilection( 90%). FMD is commoner in
whites than in blacks. The mean age of onset of hypertension 43
years.
• Familial FMD occurs in approximately 10% of patients and
autosomal dominant inheritance

8. Etiology & pathogenesis

13. Clinical features
When to suspect?
• Onset of hypertension at >55 years of age
• Accelerated, treatment resistant or malignant hypertension
• Unexplained difference in kidney size >1.5 cm
• Recurrent unexplained pulmonary edema
• Worsening renal function after ACE inhibitor treatment
• Unexplained renal dysfunction
• Evidence of peripheral artery disease or CAD

14. ASRVD (atherosclerotic renal vascular disease )
• Atherosclerotic plaque often arises in the first or second centimeter
of the renal artery or may extend from the aorta into the renal
ostium.
• Predictors of ASRVD include a history of hypertension, presence of
renal functional impairment.
• coexisting vascular or coronary artery disease, the presence of
abdominal bruits, and a history of smoking. RA lesions are bilateral in
20% to 40% of such patients.

16. Fibromuscular dysplasia (FMD)
• Fibromuscular dysplasia (FMD) is a noninflammatory,
nonatherosclerotic arteriopathy and the second most
common cause of RVH.
• It usually involves the middle to distal renal artery or
branches. The vascular distribution of FMD involves primarily
the renal and cerebral arteries.
• Renal arteries are involved with FMD in 65% to 70% of cases.
Bilateral RA disease is seen in 25% to 35% of adult cases.

18. NATURAL HISTORY
• ASRVD typically progresses over 2 to 5 years.
• Over 4 to 5 years, 6% to 16% of stenoses advance to
occlusion.
• Progression is most likely in patients with more than 60%
stenosis.
• Follow-up studies of patients with incidentally detected,
highgrade RA stenosis (>70%) treated medically indicate that
fewer than 10% required later revascularization for
intractable hypertension.
• Another report noted that few patients with incidental RA
stenosis progressed to ESRD over follow-up of 8 to 9 years.

19. • Retrospective analyses report 3-year to 5-year mortality
rates of 30% to 35% in patients with RA stenosis, largely
caused by cardiovascular events or cerebrovascular accident.
• In follow-up of more than 1200 patients who underwent
coronary and renal angiography, patients with RA stenosis
had a 65% 4-year survival versus 85% for those without RA
stenosis at catheterization.
• The 5- and 10-year survival rates for patients reaching ESRD
caused by IRD are as low as 18% and 5%, respectively

20. • It appears that up to 27% of patients may demonstrate
angiographic progression of FMD when serial studies are
undertaken.
• This appears to be limited to younger patients, with few
patients developing new or progressive lesions after age 50
years.
• FMD rarely causes ESRD unless hypertension remains
uncontrolled or thrombosis or dissection of the renal vessel
results in renal infarction.
• Renal cortical atrophy has been reported in more than half
ofpatients with untreated FMD

21. DIAGNOSIS

22. DOPPLER USG
• PSV > 180: >60 % STENOSIS
• EDV > 150: > 80 % STENOSIS
• ACCELERATION TIME : > 0.08-0.1
• RESISTIVE INDEX

23. TREATMENT
• The main aim of treatment
is to reduce cardiovascular
mortality, to improve or
stabilize renal function and
blood pressure control.
• Treatment options include
medication, surgical
reconstruction and
transluminal angioplasty
with or without stenting.

25. • Medication having proven role in preventing cardiovascular
mortality including statins, renin angiotensin antagonists,
and low dose aspirin are also effective in secondary
prevention of IN
• patients who received reninangiotensin antagonists had a
lower incidence of death and cardiovascular events, a higher
incidence of AKI and a lower incidence of long-term dialysis
than patients who did not receive such treatment

28. • Revascularization should be considered in RAS with rapid
worsening of renal function or resistant HTN (4 or more
antiHTNsive agents especially in the setting of CHF or
recurrent flash pulmonary edema).
• When the kidney size is <8.0 cm long or the RI is >0.80,
there is little chance of BP improvement or recovery of GFR.

29. • Angioplasty has a better blood pressure outcome and is thus
more strongly indicated in fibromuscular dysplasia than in
atherosclerotic RAS.
• The standard procedure for revascularization involves
balloon angioplasty, and, if necessary, stent placement.
• For patients with a macroaneurysm (an aneurysm larger
than 2 cm in diameter) or with complex lesions that affect
segmental arteries,surgical reconstruction is indicated

31. Recent studies

33. The study concluded that revascularization may be of
benefit in patients with anatomically significant RAS
who present with rapidly deteriorating renal function,
especially in the presence of severe bilateral ARVD or
<1 g/day proteinuria.

37. THANK YOU