Elevated urinary albumin excretion is associated with impaired arterial dilatory capacity in clinically healthy subjects

Abstract

Background - Elevated urinary albumin excretion (UAE) predicts atherosclerotic cardiovascular disease. It is hypothesized that elevated UAE is associated with a generalized vascular dysfunction. This study tested this hypothesis for conduit arteries. Methods and Results - Clinically healthy subjects were selected: 19 with UAE >90th percentile in the background population (6.6 μg/min <6.6 μg/min). External ultrasound was used to measure the dilatory response of the brachial artery to postischemic increased blood flow (endothelium-dependent, flow-associated dilation) and to nitroglycerin (endothelium-independent, nitroglycerin-induced dilation). Plasma concentrations of the endothelial markers nitrate/nitrite, thrombomodulin, and von Willebrand factor antigen were also measured. Both flow-associated and nitroglycerin-induced dilations were significantly impaired in subjects with elevated UAE as compared with normoalbuminuric control subjects: 102.0±1.0% (mean±SEM) versus 104.3±0.6% (P<0.05) and 120.1 ± 1.5% versus 123.8±1.0% (P<0.05). No differences in the plasma concentrations of endothelial markers were found. Conclusions - Slightly elevated UAE is associated with impaired conduit arterial dilatory capacity in clinically healthy subjects, and this impairment may be explained by a reduced dilatory response to nitric oxide of both endogenous and exogenous origin. Impaired arterial dilatory capacity may contribute to the increased cardiovascular risk in subjects with elevated UAE.