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

Background-Elevated urinary albumin excretion (UAE) predicts atheroscleroti c cardiovascular disease. It is hypothesized that elevated UAE is associate d with a generalized vascular dysfunction. This study tested this hypothesi s for conduit arteries. Methods and Results-Clinically healthy subjects were selected: 19 with UAE >90th percentile in the background population (6.6 mug/min<UAE<150 mug/min) and 41 with normoalbuminuria (UAE <6.6 <mu>g/min). External ultrasound was used to measure the dilatory response of the brachial artery to postischem ic increased blood flow (endothelium-dependent, flow-associated dilation) a nd to nitroglycerin (endothelium-independent, nitroglycerin-induced dilatio n). Plasma concentrations of the endothelial markers nitrate/nitrite, throm bomodulin. 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 sub jects: 102.0 +/-1.0% (mean +/- SEM) versus 104.3 +/-0.6% (P<0.05) and 120.1 <plus/minus>1.5% versus 123.8 +/-1.0% (P<0.05), No differences in the plasm a concentrations of endothelial markers were found. Conclusions-Slightly elevated UAE is associated with impaired conduit arter ial dilatory capacity in clinically healthy subjects, and this impairment m ay be explained by a reduced dilatory response to nitric oxide of both endo genous and exogenous origin, Impaired arterial dilatory capacity may contri bute to the increased cardiovascular risk in subjects with elevated UAE.