Renal Insufficiency and Renal Artery Occlusive Disease

Pathophysiology

The pathophysiology of ischemic nephropathy remains incompletely understood. The earliest clinical reports suggested a glomerular filtration failure based on decreased perfusion pressure within the kidney; however, the cellular and subcellular basis for ischemic nephropathy is poorly defined. Like renovascular hypertension, the renin–angiotensin system likely contributes to ischemic nephropathy through its paracrine effects, with intrarenal angiotensin peptides affecting arteriolar tone. Angiotensin peptides have also been shown to promote tubular injury and interstitial fibrosis in the presence of atherosclerotic renal artery stenosis. This observation is supported by an increase in interstitial platelet-derived growth factor β, which is associated with increased extracellular matrix and interstitial fibrosis.

In addition to these possible contributors to excretory renal insufficiency, an atherosclerotic lesion may also contribute to an irreversible loss of kidney function as a source of atheroemboli. Unfortunately, studies that distinguish potentially reversible ischemic nephropathy from irreversible renal parenchymal disease are lacking. This distinction is of significant clinical importance because recovery of kidney function after correction of atherosclerotic kidney lesions associated with ischemic nephropathy has proved to be the single strongest predictor of dialysis-free survival on follow-up.