title: No association between deletion-type angiotensin-converting enzyme gene polymorphism and left-ventricular hypertrophy in hemodialysis patients.
abstract: Left-ventricular hypertrophy (LVH), a bad prognostic sign, is a common finding in hemodialysis patients. The aim of the study was to analyze factors, including angiotensin-converting enzyme (ACE) genotype that may have an effect on the development of LVH in hemodialysis patients. Seventy-nine hemodialysis patients (42 males, 37 females, mean age 37.7 +/- 13.1 years) and 82 age- and sex-matched normotensive healthy controls (40 males, 42 females, mean age 35.6 +/- 5.7 years) were included. Left-ventricular mass index (LVMI) was higher in the hemodialysis group compared to controls (170.1 +/- 69.3 versus 84.9 +/- 15.7 g/m(2), p < 0.001). Fourty-three hypertensive patients in the hemodialysis group had an increased LVMI compared to 36 normotensive hemodialysis patients (194.2 +/- 75.5 versus 141.2 +/- 48.0 g/m(2), p < 0.001). On univariate analysis, LVMI was found to be correlated with blood pressure (r = 0.38, p < 0.001), time spent on dialysis (r = 0.22, p = 0.02) and hemoglobin levels (r = -0.21, p = 0.03). No correlation was found between LVMI and age (r = 0.09, p = 0.22), predialytic creatinine (r = 0.09, p = 0.21) and albumin (r = -0.10, p = 0.18). On multivariate analysis for the predictors of LVMI, blood pressure, time spent on dialysis and hemoglobin levels were also found to be significant. LVMI in DD, ID and II genotypes were 155.0 +/- 71.2, 181.6 +/- 60.6, and 163.6 +/- 83.4 g/m(2), respectively (p > 0.05). No association between LVMI and DD genotype was found. ACE genotype distribution was similar in hemodialysis patients and healthy controls. It was concluded that LVH in hemodialysis patients was mainly related to hypertension, anemia and time spent on dialysis and the DD genotype had no effect on LVMI in hemodialysis patients.
authors.affiliation: Department of Internal Medicine, Experimental Medicine Center, University of Istanbul, Istanbul Faculty of Medicine, Istanbul, Turkey.
authors.forename: A
authors.initials: A
authors.lastname: Yildiz
authors.forename: V
authors.initials: V
authors.lastname: Akkaya
authors.forename: A C
authors.initials: AC
authors.lastname: Hatemi
authors.forename: N
authors.initials: N
authors.lastname: Cine
authors.forename: T
authors.initials: T
authors.lastname: Tükek
authors.forename: B
authors.initials: B
authors.lastname: Görçin
authors.forename: S
authors.initials: S
authors.lastname: Demirel
authors.forename: S
authors.initials: S
authors.lastname: Türk
authors.forename: M S
authors.initials: MS
authors.lastname: Sever
mesh_terms: D000328:Adult; D001794:Blood Pressure; D004247:DNA / Q000032:analysis; D004452:Echocardiography; D005260:Female; D017353:Gene Deletion; D005838:Genotype; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000209:etiology / Q000235:genetics*; D007676:Kidney Failure, Chronic / Q000150:complications / Q000628:therapy*; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D006435:Renal Dialysis
chemical_list: D004247:DNA; D007703:Peptidyl-Dipeptidase A