title: Angiotensin-converting enzyme polymorphism in patients with terminal renal failure.
abstract: An insertion/deletion polymorphism has been described for the gene that encodes the angiotensin-converting enzyme. The deletion allele is associated with higher angiotensin-converting enzyme plasma levels, which ultimately might lead to increased angiotensin II concentrations. Because angiotensin II is a mediator for progressive renal injury, this study determined the frequency of distribution of the angiotensin-converting enzyme insertion/deletion polymorphism in 106 hemodialysis patients and in a group of 95 healthy control patients. There was no difference between the two groups as far as the distribution of the insertion and deletion allele was concerned. Of the total hemodialysis population, 26.4% exhibited the deletion/deletion genotype, as compared with 37.9% of the healthy control population. Also, when patients with terminal renal failure as a result of glomerular disease were analyzed separately, the frequency of the deletion/deletion genotype was identical to that of the control group. Furthermore, the frequency of hypertension, coronary artery disease, left ventricular hypertrophy, and dilated cardiomyopathy, were analyzed according to the angiotensin-converting enzyme genotype, but the deletion allele could not be defined as a risk factor in the study's hemodialysis population. It was therefore concluded that the angiotensin-converting enzyme insertion/deletion polymorphism is not a major risk factor for development of end-stage renal failure. Additionally, in hemodialysis patients, there is no association between the risk for cardiovascular diseases and the angiotensin-converting enzyme genotype.
authors.affiliation: Department of Nephrology, University of Vienna, Austria.
authors.forename: A
authors.initials: A
authors.lastname: Schmidt
authors.forename: H P
authors.initials: HP
authors.lastname: Kiener
authors.forename: U
authors.initials: U
authors.lastname: Barnas
authors.forename: I
authors.initials: I
authors.lastname: Arias
authors.forename: A
authors.initials: A
authors.lastname: Illievich
authors.forename: M
authors.initials: M
authors.lastname: Auinger
authors.forename: W
authors.initials: W
authors.lastname: Graninger
authors.forename: A
authors.initials: A
authors.lastname: Kaider
authors.forename: G
authors.initials: G
authors.lastname: Mayer
mesh_terms: D000328:Adult; D000368:Aged; D000483:Alleles; D002318:Cardiovascular Diseases / Q000150:complications; D005260:Female; D005838:Genotype; D006801:Humans; D007674:Kidney Diseases / Q000235:genetics; D007676:Kidney Failure, Chronic / Q000150:complications / Q000235:genetics*; D007678:Kidney Glomerulus; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D012016:Reference Values
chemical_list: D007703:Peptidyl-Dipeptidase A