Renovascular Hypertension and Ischemic Nephropathy

Marc A. Pohl

The major issues in approaching patients with renal artery stenosis relate to the role of renal artery stenosis in the management of hypertension, ie, "renovascular hypertension, " and to the potential for vascular compromise of renal function, ie, "ischemic nephropathy." Ever since the original Goldblatt experiment in 1934, wherein experimental hypertension was produced by renal artery clamping, countless investigators and clinicians have been intrigued by the relationship between renal artery stenosis and hypertension. Much discussion has focused on the pathophysiology of renovascular hypertension, the renin angiotensin system, diagnostic tests to detect presumed renovascular hypertension, and the relative merits of surgical renal revascularization (SR), percutaneous transluminal renal angioplasty (PTRA), and drug therapy in managing patients with renal artery stenosis and hypertension. Hemodynamically significant renal artery stenosis, when bilateral or affecting the artery to a solitary functioning kidney, can also lead to a reduction in kidney function (ischemic nephropathy). This untoward observation may be reversed by interventive maneuvers, eg, surgical renal revascularization, PTRA, or renal artery stenting. The syndrome of "ischemic renal disease" or "ischemic nephropathy" now looms as an important clinical condition and has attracted the fascination of nephrologists, vascular surgeons, and interventional cardiologists and radiologists.

The detection of renal artery stenosis in a patient with hypertension usually evokes the assumption that the hypertension is due to the renal artery stenosis. However, renal artery stenosis is not synonymous with "renovascular hypertension. " On the basis of autopsy studies and clinical angiographic correlations, high-grade atherosclerotic renal artery stenosis (ASO-RAS) in patients with mild blood pressure elevation or in patients with normal arterial pressure is well recognized. The vast majority of patients with ASO-RAS who have hypertension have essential hypertension, not renovascular hypertension. These hypertensive patients with ASO-RAS are rarely cured of their hypertension by interventive procedures that either bypass or

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