A meta-analysis of the association between angiotensin-converting enzyme insertion/deletion gene polymorphism and end-stage renal disease risk in IgA nephropathy patients

J Renin Angiotensin Aldosterone Syst. 2013 Sep;14(3):235-41. doi: 10.1177/1470320312459978. Epub 2012 Oct 11.

Abstract

Background and objective: The association between angiotensin-converting enzyme (ACE) insertion/deletion (I/D) gene polymorphism and end-stage renal disease (ESRD) risk in IgA nephropathy (IgAN) patients is still controversial. A meta-analysis was performed to evaluate the association between ACE I/D gene polymorphism and ESRD susceptibility in IgAN patients.

Method: A predefined literature search and selection of eligible relevant studies were performed to collect data from electronic databases.

Results: Thirteen articles were identified for the analysis of the association between ACE I/D gene polymorphism and ESRD risk in IgAN patients. D allele and DD genotype were associated with ESRD susceptibility in IgAN patients for overall populations (p=0.01 and 0.003, respectively). In Asians, there was a markedly positive association between DD genotype and ESRD susceptibility (p=0.03). Furthermore, D allele and DD genotype were associated with ESRD susceptibility in Caucasians (p=0.02 and 0.03, respectively). However, II genotype might not play a protective role against ESRD onset for overall populations, Asians and Caucasians.

Conclusion: DD homozygote is a significant genetic molecular marker for the onset of ESRD in IgAN patients.

Keywords: End-stage renal disease; IgA nephropathy; angiotensin-converting enzyme; insertion/deletion gene polymorphism; meta-analysis.

Publication types

  • Meta-Analysis

MeSH terms

  • Alleles
  • Genetic Association Studies*
  • Genetic Predisposition to Disease*
  • Glomerulonephritis, IGA / complications
  • Glomerulonephritis, IGA / enzymology
  • Glomerulonephritis, IGA / genetics*
  • Humans
  • INDEL Mutation / genetics*
  • Kidney Failure, Chronic / complications
  • Kidney Failure, Chronic / enzymology
  • Kidney Failure, Chronic / genetics*
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Genetic*
  • Publication Bias
  • Risk Factors

Substances

  • ACE protein, human
  • Peptidyl-Dipeptidase A