Erythrocyte transmembrane electron transfer in haemodialysis patients

Abstract

Background and aims Patients with chronic renal failure, especially those treated with haemodialysis, have an increased risk of developing atherosclerotic vascular disease probably as a result of enhanced oxidative stress. The human cell membrane possesses electron transfer systems which protect against extracellular pro-oxidant challenge. We evaluated (1) the erythrocyte velocity of ferricyanide reduction (RBC vfcy) in 25 uraemic patients (aged 25–71 years; 14 males), (2) the changes induced by a single haemodialysis session and (3) biomarkers of oxidative stress. Methods and results Before and after a mid-week dialysis session, we measured RBC vfcy, erythrocyte glutathione (RBC GSH), plasma and red cell membrane malondialdehyde (P and RBC MDA), plasma sulphydryl groups (P SH), plasma vitamin C levels and haemolysis percentage. Pre-dialysis RBC GSH (0.68 ± 0.13 vs 0.80 ± 0.13 mg/mL, p < 0.01), P SH (266 ± 74 vs 406 ± 78 μmol/L, p < 0.01) and plasma vitamin C (7.0 ± 5.1 vs 21.5 ± 8.5 mg/L, p < 0.001) were lower than in 25 age-sex-matched healthy controls; P MDA (1.57 ± 0.52 vs 0.54 ± 0.29 nmol/mL, p < 0.001), RBC MDA (0.42 ± 0.13 vs 0.34 ± 0.16 nmol/mL, p < 0.05) and haemolysis (1.2 ± 0.3 vs 0.7 ± 0.3%, p < 0.001) were increased. Baseline RBC vfcy did not differ from normals (13.1 ± 5.2 vs 12.9 ± 3.2 mmol/mL/h). Following dialysis, RBC vfcy (to 8.9 ± 4.5 mmol/mL/h, p < 0.001) decreased, as well as P MDA, RBC MDA and plasma vitamin C (to 2.5 ± 1.4 mg/L, p < 0.001), whereas P SH groups increased (to 413 ± 99 μmol/L, p < 0.001); haemolysis percentage remained high. RBC vfcy values were correlated to RBC GSH and vitamin C levels. Conclusions Uraemic patients showed signs of oxidative stress. Pre-dialysis RBC vfcy is maintained in the normal range on account of a reduced intracellular content of GSH and in spite of low plasma ascorbate. A single haemodialysis treatment reduced biomarkers of protein and lipid oxidation but markedly impaired transmembrane electron transfer, which could be explained by acute depletion of electron donors.