Angiotensin-I-converting enzyme insertion/deletion polymorphism and high urinary albumin concentration in French Type 2 diabetes patients

Diabet Med. 2003 Aug;20(8):677-82. doi: 10.1046/j.1464-5491.2003.01024.x.

Abstract

Aims: Family-based studies suggest a genetic basis for nephropathy in Type 2 diabetes. The angiotensin-I-converting enzyme (ACE) gene is a candidate gene for Type 1 diabetes nephropathy. We assessed the association between high urinary albumin concentration and ACE insertion/deletion (I/D) polymorphism, in French Type 2 diabetes patients.

Methods: We studied 3139 micro/macroalbuminuric French patients recruited in the DIABHYCAR Study, an ACE inhibition trial in Type 2 diabetes patients with renal and cardiovascular outcomes. The main inclusion criteria were age >/= 50 years, urinary albumin concentration >/= 20 mg/l assessed centrally during two consecutive screening visits, and plasma creatinine concentration </= 150 micro mol/l. These patients were compared with 605 normoalbuminuric (NA; urinary albumin concentration < 10 mg/l at first screening for the DIABHYCAR Study) French patients. ACE I/D genotype was determined by nested polymerase chain reaction.

Results: The ACE I/D polymorphism was in Hardy-Weinberg equilibrium. The distribution of genotypes did not differ significantly between micro/macroalbuminuric and NA patients: 552 and 115 II, 1468 and 282 ID, 1119 and 208 DD (P = 0.67). However, the ACE D allele was more frequent among normotensive micro/macroalbuminuric patients than among NA patients (P = 0.039).

Conclusions: The ACE I/D polymorphism was not associated with high urinary albumin concentration in French Type 2 diabetes patients.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Albuminuria / genetics*
  • Cross-Sectional Studies
  • Diabetes Mellitus, Type 2 / genetics*
  • Diabetic Angiopathies / genetics
  • Diabetic Nephropathies / genetics
  • Female
  • Gene Deletion*
  • Humans
  • Male
  • Middle Aged
  • Mutagenesis, Insertional / genetics*
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Genetic / genetics*

Substances

  • Peptidyl-Dipeptidase A