title: Genetic variants in hypertensive patients with coronary artery disease and coexisting atheromatous renal artery stenosis.
abstract: BACKGROUND
  Atheromatous renal artery stenosis (ARAS) often coexists with coronary artery disease (CAD). This study evaluated the prevalence of three polymorphisms: angiotensin-converting enzyme (ACE) insertion/deletion (Ins/Del), endothelial nitric oxide synthase (eNOS) Glu298Asp, and methylenetetrahydrofolate reductase (MTHFR) C677T, in hypertensive patients referred for coronary and renal angiography.
  
  
  METHODS
  The study included 223 hypertensive patients divided into three groups: 72 patients without significant CAD or evidence of ARAS, 111 patients with significant CAD but no ARAS, and 40 patients with coexisting significant CAD and evidence of ARAS. The control group consisted of 195 age- and sex-matched healthy subjects.
  
  
  RESULTS
  Patients with coexisting significant CAD and evidence of ARAS were older (p=0.03), less frequently obese (p=0.02), and more likely to have peripheral carotid or femoral artery disease (PAD) (p=0.02) compared with patients with significant CAD but no ARAS. They differed in terms of ACE Del/Del genotype distribution (40% vs. 17.1%, respectively, p=0.007). In a multivariate analysis the independent predictors of ARAS were PAD (OR: 3.7, 95%CI: 1.1-12.3, p=0.005) and ACE Del/Del polymorphism (OR: 3.3, 95%CI: 1.3-8.2, p=0.01). There was a higher prevalence of eNOS Asp/Asp genotype in all patients with significant CAD than in controls (9.3% vs. 3.6%, respectively, p=0.02), but no difference in MTHFR polymorphism between the studied groups was found.
  
  
  CONCLUSIONS
  In the hypertensive population referred for coronary and renal angiography, the ACE insertion/deletion variant but not eNOS Glu298Asp or MTHFR C677T polymorphism, seems to coexist with atheromatous renal artery stenosis.
authors.affiliation: Laboratory of Molecular Biology, Institute of Cardiology, Warsaw, Poland. mszperl@yahoo.com
authors.forename: Malgorzata
authors.initials: M
authors.lastname: Szperl
authors.forename: Zofia
authors.initials: Z
authors.lastname: Dzielinska
authors.forename: Marta
authors.initials: M
authors.lastname: Roszczynko
authors.forename: Lukasz A
authors.initials: LA
authors.lastname: Malek
authors.forename: Magdalena
authors.initials: M
authors.lastname: Makowiecka-Ciesla
authors.forename: Marcin
authors.initials: M
authors.lastname: Demkow
authors.forename: Jacek
authors.initials: J
authors.lastname: Kadziela
authors.forename: Aleksander
authors.initials: A
authors.lastname: Prejbisz
authors.forename: Elzbieta
authors.initials: E
authors.lastname: Florczak
authors.forename: Tomasz
authors.initials: T
authors.lastname: Zielinski
authors.forename: Andrzej
authors.initials: A
authors.lastname: Januszewicz
authors.forename: Witold
authors.initials: W
authors.lastname: Ruzyllo
mesh_terms: D001483:Base Sequence; D003324:Coronary Artery Disease / Q000150:complications*; D017931:DNA Primers; D005260:Female; D014644:Genetic Variation; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000235:genetics*; D008297:Male; D042965:Methylenetetrahydrofolate Reductase (NADPH2) / Q000235:genetics; D008875:Middle Aged; D015999:Multivariate Analysis; D052250:Nitric Oxide Synthase Type III / Q000235:genetics; D007703:Peptidyl-Dipeptidase A / Q000235:genetics; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D011446:Prospective Studies; D012078:Renal Artery Obstruction / Q000150:complications*
chemical_list: D017931:DNA Primers; D052250:Nitric Oxide Synthase Type III; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D007703:Peptidyl-Dipeptidase A