Pseudo renal artery stenosis (PRAS) syndrome

During the course of a long-term, prospective, randomized study in 77 hypertensive nephrosclerosis patients, five patients developed evidence suggestive of renal artery stenosis. However, arteriography demonstrated patent renal arteries. The evidence suggestive of renal artery stenosis was: (1) converting-enzyme inhibitor (CEI)-induced renal dysfunction including marked and reversible increases in serum creatinine and urea concentrations, (2) minoxidil-induced hyperreninemia despite beta-adrenoceptor blockade and volume expansion, and (3) minoxidil-induced salt and water retention with diuretic resistant edema. Thus, the renal dysfunction induced by CEI in these patients with patent renal arteries is similar to the alterations occurring in patients having bilateral renal artery stenosis. The diuretic resistant edema and the beta-adrenoceptor blocker resistant high renin release are also functional alterations of renal artery stenosis. We suspect that the long-standing and usually severe hypertension in these patients has caused sufficient arteriolar hypertrophy or sclerosis to interfere with renal blood flow and to induce these functional lesions of renal artery stenosis. With widespread use of the new CEI agents in patients with renal disease, this syndrome suggestive of renal artery stenosis may be encountered in as many as 10% of hypertensive nephrosclerosis patients during long-term treatment with converting-enzyme inhibitors.