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(Hypertension. 2004;44:448.)
© 2004 American Heart Association, Inc.

Scientific Contributions

Genetic Risk of Atherosclerotic Renal Artery Disease

The Candidate Gene Approach in a Renal Angiography Cohort

Marieke van Onna; Abraham A. Kroon; Alphons J.H.M. Houben; Derk Koster; Maurice P.A. Zeegers; Léon H.G. Henskens; Arian W. Plat; Henri E.J.H. Stoffers; Peter W. de Leeuw

From the Departments of Internal Medicine (M.v.O., A.A.K., A.J.H.M.H., L.H.G.H., P.W.d.L.) and Radiology (D.K.), University Hospital Maastricht and Cardiovascular Research Institute Maastricht (CARIM); Departments of Epidemiology (M.P.A.Z.) and General Practice (A.W.P., H.E.J.H.), Care and Public Health Research Institute (CAPHRI), Maastricht University, the Netherlands; Department of General Practice (M.P.A.Z.), Katholieke Universiteit Leuven, Leuven, Belgium.

Correspondence to Peter W. de Leeuw MD, PhD, FAHA, Department of Internal Medicine, University Hospital Maastricht, PO Box 5800, 6202 AZ Maastricht, the Netherlands. E-mail p.deleeuw{at}intmed.unimaas.nl

It is largely unknown to what extent genetic abnormalities contribute to the development of atherosclerotic renal artery disease. Among the potential candidate genes, those of the renin-angiotensin system and the endothelial nitric oxide synthase (eNOS) rank high because of their importance in the atherosclerotic process. We investigated the association of polymorphisms in these genes (the angiotensinogen Met235Thr, the angiotensin-converting enzyme insertion/deletion, the angiotensin II type-1 receptor A1166C, and the eNOS Glu298Asp) with the presence or absence of atherosclerotic renovascular disease in 456 consecutive hypertensive patients referred for renal angiography on the suspicion of renovascular hypertension. Nondiseased normotensive (n=200) and hypertensive (n=154) patients from a family practice served as external controls. Renal artery disease was present in 30% of our angiography group. The Asp allele of the eNOS Glu298Asp polymorphism was associated with atherosclerotic renal artery stenosis with an odds ratio of 1.44 (95% confidence interval 1.00 to 2.09) versus hypertensives with angiographically proven patent arteries, of 1.89 (1.24 to 2.87) versus hypertensive family practice controls, and of 2.09 (1.29 to 3.38) versus normotensive family practice controls. However, this allele also differed significantly between patients with patent renal arteries and normotensive and hypertensive controls. No differences were found with respect to the other genetic polymorphisms. We hypothesize that the Asp allele of the Glu298Asp polymorphism may predispose to the development of atherosclerotic lesions but that renal artery involvement depends on other factors, also.

Key Words: hypertension, renovascular • renal artery • polymorphism • nitric oxide synthase • renin-angiotensin system • case-control studies

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