Association of angiotensin-converting enzyme and endothelial Nitric Oxide synthase gene polymorphisms with vascular disease in ESRD patients in a Chinese population

Mol Cell Biochem. 2008 Dec;319(1-2):33-9. doi: 10.1007/s11010-008-9874-6. Epub 2008 Jul 16.

Abstract

Background: The effect of angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and endothelial Nitric Oxide synthase (eNOS) gene G894 --> T on vascular disease in end-stage renal disease (ESRD) patients was rarely studied previously. We investigated such effect in a Chinese population.

Methods: A total of 153 ESRD patients with vascular disease (88 men and 65 women; mean age +/- SD: 54.0 +/- 13.2) were recruited. Polymerase chain reaction was used to classify the ACE genotypes as II, ID and DD and the eNOS genotypes as GG, GT, and TT. Analyses were performed in ESRD patients with vascular disease (n = 153) and the age-matched controls (n = 148).

Results: The frequencies of ACE DD and eNOS TT genotypes and ACE D and eNOS T alleles in ESRD patients with vascular disease were significantly higher than those in the controls (P < 0.05). There was a significant interaction between ACE I/D alleles and eNOS G894 --> T polymorphism: adjusted odds ratio 2.128 (95%CI 1.022-4.434, P = 0.017).

Conclusions: These results indicated that the etiology of vascular disease in ESRD patients is associated with ACE and eNOS (G894 --> T) gene polymorphisms. Our data also suggest that an interaction effect may exist between ACE (I/D) and eNOS (G894 --> T) polymorphism in increasing the risk of vascular complications in ESRD patients.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Asian People
  • China
  • DNA Mutational Analysis
  • Female
  • Genotype
  • Humans
  • Kidney Failure, Chronic / complications
  • Kidney Failure, Chronic / enzymology
  • Kidney Failure, Chronic / genetics*
  • Male
  • Middle Aged
  • Mutation
  • Nitric Oxide Synthase Type III / genetics*
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Genetic*
  • Risk Factors
  • Vascular Diseases / complications
  • Vascular Diseases / enzymology
  • Vascular Diseases / genetics*

Substances

  • NOS3 protein, human
  • Nitric Oxide Synthase Type III
  • ACE protein, human
  • Peptidyl-Dipeptidase A