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.
Material and Method
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.

Keywords: Polymerase Chain Reaction, Renal Artery Obstruction - complications, Prospective Studies, Nitric Oxide Synthase Type III - genetics, Peptidyl-Dipeptidase A - genetics, Multivariate Analysis, Methylenetetrahydrofolate Reductase (NADPH2) - genetics, Hypertension - genetics, genetic variation, Polymorphism, Genetic, DNA Primers, Coronary Artery Disease - complications, Base Sequence