Complement receptor 1 gene polymorphism and cardiovascular disease in dialyzed end-stage renal disease patients

Hum Immunol. 2010 Sep;71(9):878-82. doi: 10.1016/j.humimm.2010.06.001. Epub 2010 Jun 9.

Abstract

Inflammation plays an important role in cardiovascular disease (CVD). The complement system is a critical component of innate and acquired immunity. We investigated whether the polymorphisms in the complement receptor 1 (CR1) gene are associated with CVD in end-stage renal disease (ESRD) patients. The study groups of 1200 patients with ESRD, 360 patients with type 2 diabetes and 924 healthy individuals were genotyped. The GG genotype of the C5507G polymorphism was significantly more frequent in ESRD patients with CVD than in patients without CVD and controls (odds ratio [OR] = 3.44, 95% confidence interval [CI] = 2.23-5.3, and OR = 5.46, 95% CI = 3.72-8.0, respectively). The GG genotype was observed in 62% of patients with a history of myocardial infarction. The frequency of the G allele was also higher in patients with CVD (OR = 2.24, 95% CI = 1.93-2.61 vs controls, and OR = 1.97, 95% CI = 1.63-2.36 vs patients without CVD). In the multivariate logistic regression analysis the carrier status of G allele of C5507G polymorphism was an independent risk factor of CVD in ESRD patients (p < 0.001). In conclusion, our results suggest strong association between the CR1 gene polymorphism and CVD in ESRD patients.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Amino Acid Substitution / genetics
  • Cardiovascular Diseases / complications
  • Cardiovascular Diseases / genetics*
  • Diabetes Complications / genetics
  • Diabetes Mellitus, Type 2 / genetics
  • Female
  • Gene Frequency / genetics
  • Genotype
  • Haplotypes / genetics
  • Heterozygote
  • Homozygote
  • Humans
  • Kidney Failure, Chronic / complications
  • Kidney Failure, Chronic / genetics*
  • Linkage Disequilibrium / genetics
  • Male
  • Middle Aged
  • Myocardial Infarction / etiology
  • Myocardial Infarction / genetics
  • Polymorphism, Single Nucleotide / genetics*
  • Receptors, Complement 3b / genetics*
  • Renal Dialysis*

Substances

  • CR1 protein, human
  • Receptors, Complement 3b