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Renovascular Disease and Progressive Renal Insufficiency

The importance of atherosclerotic renal artery disease as a cause of progressive renal insufficiency and end-stage renal disease (ESRD) has recently been emphasized (1, 2). The most precise terminology for this clinical entity has been debated. The terms ischemic nephropathy and ischemic renal disease have often been used; however, experimental studies have not clearly demonstrated evidence of whole kidney ischemia in chronically underperfused kidneys although localized renal ischemia to critical areas cannot be excluded (3). Alternatively, the term renovascular renal failure has been used suggesting that renal failure is due to renovascular disease, analogous to renovascular hypertension where hypertension is due to renovascular disease. In this review, we will utilize the term critical renovascular disease (RVD) or azotemic RVD to refer to this clinical entity. Many prefer to restrict this term to bilateral critical RVD causing renal insufficiency. However, it is often difficult to clearly define a cause and effect relationship between anatomic renal artery disease and renal insufficiency. The only precise way to do this may be by measuring the renal functional response to correction of the disease. The most inclusive definition of critical RVD would include critical main renal artery disease in combination with renal insufficiency, without necessarily showing a clear cut cause-and-effect relationship (4). For the purpose of this review, critical RVD includes bilateral critical renal artery atherosclerosis or critical stenosis to a solitary kidney associated with renal insufficiency. In addition, an occasional patient with unilateral disease will achieve retrieval of renal function after intervention. As will be discussed, the frequency of critical RVD is not well defined. Invasive procedures such as renal artery repair may improve renal function, delay progression of disease, and even remove pa-