(Hypertension. 1999;34:1097-1100.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
Genetic Polymorphisms of the Renin-Angiotensin System and Atheromatous Renal Artery Stenosis
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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