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Vascular function of the peripheral circulation in patients with nephrosis

Watts, G.F., Herrmann, S., Dogra, G.K., Playford, D.A., Best, J.D., Thomas, M.A.B. and Irish, A. (2001) Vascular function of the peripheral circulation in patients with nephrosis. Kidney International, 60 (1). pp. 182-189.

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Background. Nephrotic syndrome is associated with abnormal lipoprotein metabolism and increased risk of coronary heart disease. Endothelial dysfunction, an early phase of atherogenesis that manifests as impaired flow-mediated dilation (FMD) of the peripheral circulation, may link these associations. Methods. We examined endothelial function of the brachial artery and forearm resistance arteries in 15 patients with nephrosis (NP), 15 patients with primary hyperlipidemia (HL) alone, and 15 normolipidemic, nonproteinuric subjects (NC) matched for age, sex, and weight. The NP and HL groups had similar serum cholesterol and triglyceride concentrations. Postischemic FMD (endothelium-dependent) and glyceryl trinitrate-mediated dilation (GTNMD; endothelium-independent) of the brachial artery were studied using ultrasonography and computerized edge detection software. Postischemic forearm blood flow was also measured using plethysmography. Results. Postischemic FMD of the brachial artery was significantly lower in the NP and HL groups compared with NC group (mean ± SE): NP 4.91 ± 0.8%, HL 4.53 ± 0.6%, NC 8.45 ± 0.5% (P < 0.001). There were no significant differences among the groups in baseline diameter and GTNMD of the brachial artery, nor in maximal forearm blood flow and flow debt repayment of the forearm microcirculation. Significant differences in FMD among the groups were principally related to differences in serum low-density lipoprotein cholesterol. Conclusions. Patients with NP have abnormal endothelium-dependent but preserved endothelium-independent dilation of the brachial artery following an ischemic stimulus. Postischemic forearm microcirculatory function is unimpaired. Dyslipoproteinemia is probably the principal cause of endothelial dysfunction of conduit arteries in patients with NP and the basis for their increased risk of cardiovascular disease.

Item Type: Journal Article
Publisher: Nature Publishing Group
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