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

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 microgram/min<UAE<150 microgram/min) and 41 with normoalbuminuria (UAE <6.6 microgram/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.