title: Insertion/deletion polymorphism in intron 16 of the ACE gene and left ventricular hypertrophy in patients with end-stage renal disease.
abstract: We studied the relationship between polymorphism in intron 16 of the angiotensin-converting enzyme (ACE) gene and left ventricular (LV) hypertrophy in uremic patients treated with hemodialysis therapy. The LV parameters were not different for age-, hematocrit-, and blood pressure-matched patients in DD, ID, and II genotype groups. The most important factor for LV hypertrophy was systolic blood pressure, which correlated with the posterior wall thickness (r=0.35; P=0.001) and LV mass index (LVMI; r=0.23; P=0.032). Among nonhypertensive patients, the frequency of interventricular septum (IVS) hypertrophy (>12 mm) and hypertrophy in LVMI (>145 g/m2) was significantly greater in patients with the DD genotype than in I allele-positive (+) patients. The odds rate for IVS hypertrophy was 5.04 (95% confidence interval, 1.15 to 24.8). These data suggest that the DD genotype of the ACE gene polymorphism is a contributory factor for the development of LV hypertrophy in patients with end-stage renal disease (ESRD).
authors.affiliation: Department of Nephrology and Cardiology, Kasukabe Shuwa Hospital, Saitama, Japan. osono@ksh.smds.co.jp
authors.forename: E
authors.initials: E
authors.lastname: Osono
authors.forename: S
authors.initials: S
authors.lastname: Kurihara
authors.forename: N
authors.initials: N
authors.lastname: Hayama
authors.forename: Y
authors.initials: Y
authors.lastname: Sakurai
authors.forename: K
authors.initials: K
authors.lastname: Ohwada
authors.forename: N
authors.initials: N
authors.lastname: Onoda
authors.forename: M
authors.initials: M
authors.lastname: Takeuchi
authors.forename: T
authors.initials: T
authors.lastname: Tomizawa
authors.forename: Y
authors.initials: Y
authors.lastname: Komaba
authors.forename: K
authors.initials: K
authors.lastname: Hashimoto
authors.forename: S
authors.initials: S
authors.lastname: Matsunobu
authors.forename: H
authors.initials: H
authors.lastname: Yoneshima
authors.forename: Y
authors.initials: Y
authors.lastname: Iino
mesh_terms: D000367:Age Factors; D000483:Alleles; D001794:Blood Pressure; D016022:Case-Control Studies; D016001:Confidence Intervals; D004452:Echocardiography; D005260:Female; D017353:Gene Deletion; D005838:Genotype; D006346:Heart Septum / Q000000981:diagnostic imaging / Q000473:pathology; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000473:pathology; D006400:Hematocrit; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000201:enzymology / Q000235:genetics* / Q000473:pathology; D007438:Introns / Q000235:genetics*; D007676:Kidney Failure, Chronic / Q000235:genetics* / Q000628:therapy; D008297:Male; D008875:Middle Aged; D016254:Mutagenesis, Insertional; D016017:Odds Ratio; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics*; D006435:Renal Dialysis; D014511:Uremia / Q000235:genetics / Q000628:therapy
chemical_list: D007703:Peptidyl-Dipeptidase A