Endothelin-1 plasma levels in hemodialysis treatment - The influence of type 2 diabetes

Abstract

In patients on chronic hemodialysis the prevalence of atherosclerosis is increased and is by far the leading cause of morbidity and mortality. Endothelin-1, an endothelium-derived peptide with vasoconstrictive and mitogenic effects on vascular smooth muscles, is involved in the pathogenesis of atherosclerosis. The aim of the present study was to investigate the time course of plasma endothelin-1 levels during a hemodialysis session and to explore the influence of preexisting type 2 diabetes mellitus. Forty-five clinically stable hemodialysis patients (21 females, 24 males; mean age 62 ± 12 years) were evaluated. Patients with type 2 diabetes (n = 11) were compared with the group of patients without diabetes (n = 34). Relative blood volume (BV) changes (hemoglobinometry) and blood pressure (BP) was measured. Samples were taken before, every hour during, and after hemodialysis. Plasma endothelin-1 levels were measured by enzyme-linked immunoassay (ELISA) and results were corrected according to hemoconcentration. Hemodialysis with an ultrafiltration of 2215 ± 952 mL was performed. Total BV at the end of hemodialysis was 89.3% ± 8.3% of the pretreatment volume. Plasma endothelin-1 was enhanced in hemodialysis patients compared to normal subjects and increased from 1.28 ± 0.47 before to 1.44 ± 0.54 pg/mL (ref. 0.3-0.9) at the end of hemodialysis (p < 0.05). The BV change (r = 0.41) and the BP (mean BP: r = 0.34) correlated with plasma endothelin-1 at the end of hemodialysis (p < 0.05). The levels of endothelin-1 were significantly higher in the group of dialysis patients with type 2 diabetes compared to nondiabetics in all measurements (p < 0.05). These findings suggest a potential role of endothelin-1 in the pathogenesis of vascular dysfunction in diabetes mellitus. The dialysis procedure per se, through vasoconstriction due to BV decrease, local endothelial injury (a.v. fistula), or bioincompatibility reactions (foreign surface contact) may additionally alter endothelial cell functions. Copyright © 2005 Taylor & Francis Inc.