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(Hypertension. 1999;34:1097-1100.)
© 1999 American Heart Association, Inc.

Scientific Contributions

Genetic Polymorphisms of the Renin-Angiotensin System and Atheromatous Renal Artery Stenosis

Oliviero Olivieri; Elisabetta Trabetti; Silvia Grazioli; Chiara Stranieri; Simonetta Friso; Domenico Girelli; Carla Russo; Pier Franco Pignatti; Giancarlo Mansueto; Roberto Corrocher

From the Department of Clinical and Experimental Medicine, Chair of Internal Medicine (O.O., S.G., S.F., D.G., C.R., R.C.), Institute of Biology and Genetics (E.T., C.S., P.F.P.), and Institute of Radiology (G.M.), University of Verona, Verona, Italy.

Correspondence to Oliviero Olivieri, Department of Clinical and Experimental Medicine, Cattedra di Medicina Interna, Università di Verona, Policlinico Borgo Roma, 37134 Verona, Italy. E-mail olivieri{at}cmib.univr.it

Abstract—Genes that influence the renin-angiotensin system have been investigated in recent years as potential etiologic candidates of cardiovascular and renal diseases. In atheromatous renal artery stenosis (RAS), a condition characterized by persistent activation of the renin-angiotensin system, the study of these genes may be of particular relevance. We evaluated angiotensin-converting enzyme (ACE) insertion/deletion, angiotensinogen (AGT) M235T, and angiotensin II receptor (ATR) A1166C polymorphisms in relation to the occurrence of RAS. We studied 58 patients with angiographically documented RAS; 102 normotensive subjects with normal coronary arteries and no history or clinical or instrumental evidence of atherosclerosis in other vascular districts were considered the control group. Patients had a significantly higher D allele frequency (0.70 versus 0.55; ² 6.88, P=0.01; odds ratio [OR] 1.9, 95% CI 1.17 to 3.07) than did the control population; 48.3% of patients were homozygous for DD (² 6.62, P<0.05; OR 2.04, 95% CI 1.05 to 3.95); and only 8.6% carried the II genotype (OR 0.34, 95% CI 0.19 to 1.47). No significant association was found for AGT M235T and ATR A1166C. Our results suggest a predisposing role for ACE genetic polymorphism in the development and progression of atheromatous RAS.

Key Words: renal artery • angiotensin-converting enzyme • angiotensinogen • angiotensin II receptor • polymorphism

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