Erythrocyte transmembrane electron transfer in haemodialysis patients

Background and aimsPatients 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 resultsBefore 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.ConclusionsUraemic 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.