Insertion/deletion polymorphism in intron 16 of the ACE gene and left ventricular hypertrophy in patients with end-stage renal disease

Am J Kidney Dis. 1998 Nov;32(5):725-30. doi: 10.1016/s0272-6386(98)70126-x.

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).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Age Factors
  • Alleles
  • Blood Pressure
  • Case-Control Studies
  • Confidence Intervals
  • Echocardiography
  • Female
  • Gene Deletion*
  • Genotype
  • Heart Septum / diagnostic imaging
  • Heart Septum / pathology
  • Heart Ventricles / diagnostic imaging
  • Heart Ventricles / pathology
  • Hematocrit
  • Humans
  • Hypertrophy, Left Ventricular / diagnostic imaging
  • Hypertrophy, Left Ventricular / enzymology
  • Hypertrophy, Left Ventricular / genetics*
  • Hypertrophy, Left Ventricular / pathology
  • Introns / genetics*
  • Kidney Failure, Chronic / genetics*
  • Kidney Failure, Chronic / therapy
  • Male
  • Middle Aged
  • Mutagenesis, Insertional*
  • Odds Ratio
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Genetic / genetics*
  • Renal Dialysis
  • Uremia / genetics
  • Uremia / therapy

Substances

  • Peptidyl-Dipeptidase A