Angiotensin-converting enzyme gene polymorphism in chronic allograft nephropathy

Transplant Proc. 2006 Jun;38(5):1327-8. doi: 10.1016/j.transproceed.2006.02.112.

Abstract

Angiotensin causes an increased activity of hypertrophic and fibrotic processes, which similarly develop in the walls of small vessels of a renal graft during chronic rejection. In this context, the angiotensin-converting enzyme (ACE) gene, associated with increased angiotensin production, has been the subject of studies on renal diseases. The present study evaluated the influence of the ACE gene deletion polymorphism in chronic allograft nephropathy. We evaluated 240 renal transplant recipients including, 119 with normal renal function and 121 with chronic allograft nephropathy. The polymorphism was determined by polymerase chain reaction and genotyping performed after electrophoresis in 1.5% agarose gels stained with ethidium bromide. The frequency of the polymorphic allele was similar in both groups of patients. Furthermore, no significant effect of genotype was observed in chronic allograft nephropathy. Therefore, in this study, we observed no influence of the ACE gene polymorphism in chronic allograft nephropathy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Child
  • Child, Preschool
  • Chronic Disease
  • Creatinine / blood
  • Cross-Sectional Studies
  • Follow-Up Studies
  • Gene Frequency
  • Humans
  • Kidney Transplantation / pathology*
  • Kidney Transplantation / physiology*
  • Middle Aged
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Genetic*
  • Retrospective Studies
  • Transplantation, Homologous

Substances

  • Creatinine
  • Peptidyl-Dipeptidase A