Angiotensin-converting enzyme gene insertion/deletion polymorphism and left ventricular hypertrophy in hemodialysis patients

Jpn Heart J. 1997 Nov;38(6):821-30. doi: 10.1536/ihj.38.821.

Abstract

The relationships between angiotensin-converting enzyme (ACE) gene insertion (I) / deletion (D) polymorphism and left ventricular hypertrophy induced by hypertension or idiopathic hypertrophic cardiomyopathy have been studied. However, little is known about the association between this polymorphism and left ventricular hypertrophy induced by volume overload. The relationship between left ventricular hypertrophy and the ACE gene I/D polymorphism was examined in 80 maintenance hemodialysis patients (mean age: 60.1+/-1.4 <SEM> years). Multivariate regression analysis showed that the left ventricular mass index calculated by M-mode echocardiography was associated with serum creatinine (p = 0.040), male gender (p = 0.027), antihypertensive drug treatment (p = 0.026), weight gain between hemodialysis (p = 0.018) and mean blood pressure after hemodialysis (p=0.010), but not with ACE I/D genotype (p = 0.69). These findings suggest that although hemodialysis patients seem to be under volume overload, ACE genotype may not be involved in their left ventricular hypertrophy. Hypertension and other factors related to renal failure are involved in the left ventricular hypertrophy in chronic hemodialysis patients.

Publication types

  • Clinical Trial
  • Randomized Controlled Trial

MeSH terms

  • Adult
  • Aged
  • DNA Transposable Elements
  • Echocardiography
  • Female
  • Gene Deletion
  • Genotype
  • Humans
  • Hypertension / complications
  • Hypertrophy, Left Ventricular / diagnostic imaging
  • Hypertrophy, Left Ventricular / enzymology
  • Hypertrophy, Left Ventricular / genetics*
  • Kidney Diseases / complications
  • Kidney Diseases / therapy
  • Male
  • Middle Aged
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Genetic*
  • Regression Analysis
  • Renal Dialysis*

Substances

  • DNA Transposable Elements
  • Peptidyl-Dipeptidase A