Ischemic nephropathy

Abstract

Term “ischemic nephropathy” (IN) means impairment of renal function beyond occlusive disease of the main renal arteries. Time to ESRD or death does not correlate with renovascular anatomy despite vessels showing varying presentation from non occlusion to stenosis of varying degree. The parenchymal injury is multifactorial in origin ranging from cholesterol emboli, long-standing hypertension to prolonged ischemic damage. Time to intervention in RAS is challenging as efforts must be made at a stage when these ischemic changes are reversible and much before parenchymal injury can happen. The predictors of renal improvement are also still elusive. Unexplained renal failure in the background of uncontrolled hypertension, CAD or PVD or renal function worsening following use of angiotensin-converting enzyme inhibitor (ACEI), flash pulmonary edema are clinical situations associated with IN. 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. Revascularization should be considered in RAS with rapid worsening of renal function or resistant HTN (four or more antihypertensive 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. Medication having proven role in preventing cardiovascular mortality including statins, renin–angiotensin antagonists, and low dose aspirin are also effective secondary prevention of IN.