title: Atherosclerosis and the Glu298Asp polymorphism of the eNOS gene in white patients with end-stage renal disease.
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.
authors.affiliation: CNR-IBIM, National Research Council-Institute of Biomedicine, Clinical Epidemiology and Physiopathology of Renal Diseases and Hypertension, Reggio, Calabria, Italy.
authors.forename: Belinda
authors.initials: B
authors.lastname: Spoto
authors.forename: Francesco A
authors.initials: FA
authors.lastname: Benedetto
authors.forename: Alessandra
authors.initials: A
authors.lastname: Testa
authors.forename: Giovanni
authors.initials: G
authors.lastname: Tripepi
authors.forename: Francesca
authors.initials: F
authors.lastname: Mallamaci
authors.forename: Renke
authors.initials: R
authors.lastname: Maas
authors.forename: Rainer H
authors.initials: RH
authors.lastname: Boeger
authors.forename: Carmine
authors.initials: C
authors.lastname: Zoccali
authors.forename: Rosa Maria
authors.initials: RM
authors.lastname: Parlongo
authors.forename: Anna
authors.initials: A
authors.lastname: Pisano
mesh_terms: D000368:Aged; D001120:Arginine / Q000031:analogs & derivatives / Q000097:blood; D050197:Atherosclerosis / Q000097:blood / Q000235:genetics* / Q000473:pathology; D002339:Carotid Arteries / Q000473:pathology; D002340:Carotid Artery Diseases / Q000097:blood / Q000235:genetics / Q000473:pathology; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood / Q000235:genetics* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D052250:Nitric Oxide Synthase Type III / Q000235:genetics*; D011110:Polymorphism, Genetic; D012044:Regression Analysis; D017539:Tunica Intima / Q000473:pathology; D017540:Tunica Media / Q000473:pathology; D044465:White People / Q000235:genetics
chemical_list: C018524:N,N-dimethylarginine; D001120:Arginine; C496314:NOS3 protein, human; D052250:Nitric Oxide Synthase Type III