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Titolo:
Renal function in relation to three candidate genes
Autore:
Wang, JG; Staessen, JA; Tizzoni, L; Brand, E; Birkenhager, WH; Fagard, R; Herrmann, SM; Bianchi, G;
Indirizzi:
Katholieke Univ Leuven, Hypertnesie Cardiovasc Revalidatie Eenheid, Dept Mol Cardiovasc Onderzoek, Louvain, Belgium Katholieke Univ Leuven Louvain Belgium vasc Onderzoek, Louvain, Belgium Univ Milan, Div Nefrol Dialisi & Ipertens, Osped San Raffaele, Dipartimento Sci & Techol Biomed, Milan, Italy Univ Milan Milan Italy , Dipartimento Sci & Techol Biomed, Milan, Italy Free Univ Berlin, Klinikum Benjamin Franklin, D-12200 Berlin, Germany FreeUniv Berlin Berlin Germany D-12200 ranklin, D-12200 Berlin, Germany Erasmus Univ, Rotterdam, Netherlands Erasmus Univ Rotterdam NetherlandsErasmus Univ, Rotterdam, Netherlands
Titolo Testata:
AMERICAN JOURNAL OF KIDNEY DISEASES
fascicolo: 6, volume: 38, anno: 2001,
pagine: 1158 - 1168
SICI:
0272-6386(200112)38:6<1158:RFIRTT>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
ANGIOTENSIN-CONVERTING-ENZYME; ALPHA-ADDUCIN; ESSENTIAL-HYPERTENSION; DIABETIC NEPHROPATHY; INSERTION/DELETION POLYMORPHISM; BLOOD-PRESSURE; ASSOCIATION; DISEASE; SYSTEM; RISK;
Keywords:
alpha-adducin gene; angiotensin-converting enzyme (ACE); aldosterone synthase; chronic renal disease; genetic mechanisms; renal function;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Staessen, JA Catholic Univ Louvain, Study Coordinating Ctr, Lab Hypertens,Campus Gasthuisberg,Herestr 49, B-3000 Louvain, Belgium Catholic Univ Louvain Campus Gasthuisberg,Herestr 49 Louvain Belgium B-3000
Citazione:
J.G. Wang et al., "Renal function in relation to three candidate genes", AM J KIDNEY, 38(6), 2001, pp. 1158-1168

Abstract

We recently found that femoral intima media thickness, as well as the incidence of hypertension, is influenced by genes encoding the angiotensin-converting enzyme (ACE, insertion/deletion [I/D]) polymorphism, a-adducin (Gly460Trp), and aldosterone synthase (-344C/T). By interfering with blood pressure or sodium homeostasis, these genetic polymorphisms also may change renal function. We therefore investigated serum creatinine level, calculated and measured creatinine clearances, and 24-hour urinary protein excretion in subjects previously genotyped for these three polymorphisms. The 1,454 participants drawn at random from the population (64.3% of those invited) were aged 43.4 years and included 744 women (51.2%). Blood pressure, measured bystudy nurses at subjects' homes, averaged 123/76 mm Hg. Mean values were 90 mu mol/L for serum creatinine; 84 and 88 mL/min/1.73 m(2) for calculated and measured (n = 855) creatinine clearances, respectively; and 90 mg/d of protein for proteinuria (n = 556). The prevalence of mild renal dysfunction(creatinine clearance less than or equal to 60 mL/min/1.73 m(2)) was nearly 11%. In single-gene analyses with adjustment for significant covariables,the risk for mild renal dysfunction was positively associated with the ACED allele. However, multiple-gene analyses showed that these associations were restricted to carriers of the mutated alpha -adducin Trp allele (40.1% of all subjects). Findings remained similar after hypertensive patients andwomen on hormonal therapy were excluded. In this phenotypically more homogeneous subgroup, serum creatinine level was 3.6 mu mol/L (P = 0.02) and relative risks for mild renal dysfunction and proteinuria were 1.7-fold (P < 0.001) and 26% (P = 0.02) greater in ACE D subjects than ACE II homozygotes,respectively. The aldosterone synthase T allele did not strengthen geneticassociations with the ACE D allele considered alone or in combination withthe alpha -adducin Trp allele. Thus, in the present cross-sectional analysis, renal function was slightly but consistently impaired when both the ACED and alpha -adducin Trp alleles were present. These findings, together with experimental studies and our previous reports on femoral intima media thickness and the incidence of hypertension, constitute a growing body of evidence delineating a clinical entity genetically determined by the risk-carrying ACE D and a-adducin Trp alleles. (C) 2001 by the National Kidney Foundation, Inc.

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Documento generato il 29/03/20 alle ore 15:00:09