Atherosclerosis and the Glu298Asp polymorphism of the eNOS gene in white patients with end-stage renal disease

Am J Hypertens. 2005 Dec;18(12 Pt 1):1549-55. doi: 10.1016/j.amjhyper.2005.06.007.

Abstract

Background: We investigated whether the eNOS G/T polymorphism (Glu298Asp variant) is linked to the severity of carotid atherosclerosis and whether it is independent of asymmetric dimethylarginine (ADMA) in determining vascular damage in patients with end-stage renal disease (ESRD).

Methods: The eNOS polymorphism, ADMA, carotid intima-media thickness (IMT), and carotid artery (CCA) wall-to-lumen ratio (an indicator of arterial remodeling) were determined/measured in 131 patients with ESRD.

Results: Both in the co-dominant and dominant model approach, IMT as well as CCA wall-to-lumen ratio were directly related to the T allele (P < or = .009) and these relationships held true in multiple linear regression analyses including ADMA and traditional and emerging risk factors. The relationship between eNOS genotypes and CCA wall-to-lumen ratio was further analyzed by a categorical approach and in a multiple logistic regression analysis, the odds ratio (OR) of increased CCA wall-to-lumen ratio was strongly associated to the T allele (codominant model: GG, OR = 1; GT, OR = 2.1; TT, OR = 8.2; P for trend = .01; dominant model: GG, OR = 1; GT and TT, OR = 2.7; P = .02).

Conclusions: The T allele of eNOS gene is an independent predictor of intimal lesions and vascular remodeling and it is associated with the severity of atherosclerosis independently of ADMA.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Arginine / analogs & derivatives
  • Arginine / blood
  • Atherosclerosis / blood
  • Atherosclerosis / genetics*
  • Atherosclerosis / pathology
  • Carotid Arteries / pathology
  • Carotid Artery Diseases / blood
  • Carotid Artery Diseases / genetics
  • Carotid Artery Diseases / pathology
  • Female
  • Gene Frequency
  • Genotype
  • Humans
  • Kidney Failure, Chronic / blood
  • Kidney Failure, Chronic / genetics*
  • Kidney Failure, Chronic / pathology
  • Male
  • Middle Aged
  • Nitric Oxide Synthase Type III / genetics*
  • Polymorphism, Genetic
  • Regression Analysis
  • Tunica Intima / pathology
  • Tunica Media / pathology
  • White People / genetics

Substances

  • N,N-dimethylarginine
  • Arginine
  • NOS3 protein, human
  • Nitric Oxide Synthase Type III