Association of Angiotensin I Converting Enzyme Gene Polymorphism with Reflux Nephropathy in Children

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Abstract

Deletion polymorphism of angiotensin I converting enzyme (ACE) gene has been studied as a risk factor in various cardiovascular diseases and chronic nephropathies. Perturbation of local and systemic renin-angiotensin systems is one of the possible mechanisms of the progression of reflux nephropathy. In this study, the implication of ACE gene polymorphism in renal scarring and deterioration of renal function was analyzed in 66 children with vesicoureteral reflux. The genotype for the polymorphism was determined by PCR, and renal scar was identified by <sup>99m</sup>Tc-DMSA renal scan. The allelic frequency of the deletion polymorphism showed no significant difference either between patients with normal renal function and those with decreased renal function or between patients with renal scar and those without. We conclude that deletion polymorphism of ACE gene, as an independent variable, is not associated with reflux nephropathy in children with vesicoureteral reflux.

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A prospective evaluation of an angiotensin-converting-enzyme gene polymorphism and the risk of ischemic heart disease.

K Lindpaintner, M Pfeffer, R. Kreutz … (1995)

In a previous study, men with a history of myocardial infarction were found to have an increased prevalence of homozygosity for the deletional allele (D) of the angiotensin-converting-enzyme (ACE) gene. The D allele is associated with higher levels of ACE, which may predispose a person to ischemic heart disease. We investigated the association between the ACE genotype and the incidence of myocardial infarction, as well as other manifestations of ischemic heart disease, in a large, prospective cohort of U.S. male physicians. In the Physicians' Health Study, ischemic heart disease as defined by angina, coronary revascularization, or myocardial infarction developed in 1250 men by 1992. They were matched with 2340 controls according to age and smoking history. Zygosity for the deletion-insertion (D-I) polymorphism of the ACE gene was determined by an assay based on the polymerase chain reaction. Data were analyzed for both matched pairs and unmatched samples, with adjustment for the effects of known or suspected risk factors by conditional and nonconditional logistic regression, respectively. The ACE genotype was not associated with the occurrence of either ischemic heart disease or myocardial infarction. The adjusted relative risk associated with the D allele was 1.07 (95 percent confidence interval, 0.96 to 1.19; P = 0.24) for ischemic heart disease and 1.05 (95 percent confidence interval, 0.89 to 1.25; P = 0.56) for myocardial infarction, if an additive mode of inheritance is assumed. Additional analyses assuming dominant and recessive effects of the D allele also failed to show any association, as did the examination of low-risk subgroups. In a large, prospectively followed population of U.S. male physicians, the presence of the D allele of the ACE gene conferred no appreciable increase in the risk of ischemic heart disease or myocardial infarction.

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Angiotensin-converting enzyme DD genotype in patients with ischaemic or idiopathic dilated cardiomyopathy.

William T. Abraham, Sarah C. Taft, S. Perryman … (1993)

Polymorphism in the angiotensin-converting enzyme (ACE) gene has been shown to correlate with circulating ACE concentrations, and also to be an independent risk factor for the development of myocardial infarction, particularly in men thought to be at low risk by standard criteria. We determined the genotypes of individuals with end-stage heart failure due to either ischaemic dilated cardiomyopathy (102) or idiopathic dilated cardiomyopathy (112) and compared these to organ donors with normally functioning hearts (79). Genotypes were determined by the polymerase chain reaction with oligonucleotide primers flanking the polymorphic region in intron 16 of the ACE gene to amplify template DNA isolated from patients. Compared with the DD frequency in the control population, the frequency of the ACE DD genotype was 48% higher in individuals with idiopathic dilated cardiomyopathy (p = 0.008) and 63% higher in subjects with ischaemic cardiomyopathy (p = 0.008), suggesting that an ACE gene variant may contribute to the pathogenesis of both types of cardiomyopathy.

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Author and article information

Journal

Journal ID (publisher-id): NEF

Journal ID (nlm-ta): Nephron

Journal ID (doi): 10.1159/issn.1660-8151

Title: Nephron

Publisher: S. Karger AG

ISSN (Print): 1660-8151

ISSN (Electronic): 2235-3186

Publication date Subscription-year: 2000

Publication date (Print): September 2000

Publication date (Electronic): 30 August 2000

Volume: 86

Issue: 1

Pages: 52-55

Affiliations

Departments of Pediatrics, ^aBoramae Hospital, Seoul National University College of Medicine, ^bSanggye Paik Hospital, Inje University, and ^cSeoul National University College of Medicine, Seoul, Korea

Article

Publisher ID: 45712 Other ID: Nephron 2000;86:52–55

DOI: 10.1159/000045712

PubMed ID: 10971153

SO-VID: 7bb53705-0371-485f-8b5c-bd6e0cc93a48

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Association of Angiotensin I Converting Enzyme Gene Polymorphism with Reflux Nephropathy in Children

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Karger: Nephrology

Most cited references 2

A prospective evaluation of an angiotensin-converting-enzyme gene polymorphism and the risk of ischemic heart disease.

Angiotensin-converting enzyme DD genotype in patients with ischaemic or idiopathic dilated cardiomyopathy.

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