Renovascular Disease Daniel Shoskes MD, MSc, FRCSC Professor of Surgery/Urology Glickman Urological and Kidney Institute Cleveland Clinic.

Renovascular Disease

Daniel Shoskes MD, MSc, FRCSC

Professor of Surgery/Urology

Glickman Urological and Kidney Institute

Cleveland Clinic

• Pathophysiology

• Classification of Lesions

• Clinical Evaluation

• Medical and Surgical Management

• Renal Artery Aneurysm

Overview

Goldblatt Dog Models

ARB/ACE inhibitors help Only help when Na depleted

Ischemic Nephropathy

• Does not correlate with hypertension

• Progressive azotemia in pt with risk factors

for atherosclerotic disease

• Progresses through nephrosclerosis and

atheroemboli

• Treatment of hypertension will not improve

renal function, may actually exacerbate

Diameter and Blood Flow

• Atherosclerotic (70%)

• Fibromuscular Disease (30%)

Classification

Fibromuscular Disease

Medial Fibroplasia: 77%

Perimedial Fibroplasia: 10%

Intimal Fibroplasia: 10%

Fibromuscular Hyperplasia: 3%

Atherosclerosis

• typically a systemic disease

• involves proximal 2 cm of artery

• may only be seen on oblique views

• progression common, at least 50% in 2 years

• 10-15% progress to occlusion

• can cause hypertension and Renal Failure

Medial Fibroplasia

• most common fibrous

• women 25-50

• commonly bilateral

• "string of beads"

• involves distal 2/3 and

branches

• progression less

common

Clinical Clues to RVH

• HTN onset < 30 yrs or > 55

• sudden onset, short duration

• lack of family history

• difficult to control

• malignant crisis

• bruits

• disseminated atherosclerotic disease

• renal size disparity

Key Diagnostic Points• Captopril provocation

– reduction of GFR detected by nuclear scan• best predictor of surgical cure (spec 93-98%)

– increased PRA (off most drugs)• Renal Vein Renins

– ipsilateral hypersecretion, contralateral suppression– best for bilateral disease

• Ultrasound– operator dependent, independent of renal function

• MRA – poor images beyond main renal artery

Investigation of Ischemic Nephropathy

• High suspicion

– straight to angiography

• Mild to Moderate suspicion

– non-invasive imaging (local preference)

– if significant azotemia, US rather than MRA or

spiral CT

Investigation of RVH

• High suspicion– angiography and Renal Vein Renins if bilateral

• Moderate suspicion– captopril nuclear renography (can do "post"

study first)– positive -> angio– equivocal -> non-invasive imaging– negative -> stop

Treatment of RVH

• Select medical management based on risk of ischemic nephropathy and lesion progression

– medial fibroplasia and atherosclerotic (without ischemic nephropathy) best for medical

• angioplasty +/- stents usually procedure of choice unless

– branch vessel disease

– renal artery aneurysm

• Nephrectomy if small and non-functioning

Treatment of Ischemic Nephropathy

• No benefit with unilateral disease• Signs of reversibility

– progressive occlusion– collaterals– retrograde arterial filling– size > 9 cm– Cr < 4.0– preservation of glomeruli on biopsy

Surgical Approaches

• Hepatorenal

• Splenorenal

• Ileorenal

• Autotransplant

• Arteriotomy

• Aortorenal

• Thoracic aorta - renal

Renal Artery Aneurysms

• most small and asymptomatic• pathology

– saccular (most common), fusiform, dissecting, intrarenal

• risk of rupture– absent/incomplete calcification, >2cm diameter,

expanding, hypertension, pregnancy

• other complications– pain, hematuria, dissection, emboli