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EWA KWIATKOWSKA


THE INFLUENCE OF RENAL FAILURE AND RENAL REPLACEMENT
THERAPY ON THE ACTIVITY OF ERYTHROCYTE SODIUM-PROTON
EXCHANGER

Summary
Glucose metabolism in erythrocytes (RBC) is the source of NADPH and other reducing equivalents necessary to maintain normal levels of reduced glutathione (GSH) which plays a crucial role in the defense against oxidative stress. In haemodialyzed (HD) patients, oxidation reactions dominate over defense reactions. The use of dialysis fluid without glucose can contribute to such an imbalance. Decreased activity of the sodium-proton exchanger (NHE) is one of the results of reactive oxygen forms acting on RBC. The present study enrolled 49 patients haemodialyzed with a glucose-free dialysis fluid, 26 patients haemodialyzed with 5 mmol/L glucose in the dialysis fluid and 48 controls. NHE activity in RBC was measured using Orlow’s method. GSH concentration in RBC was determined with a spectrophotometer. For in vitro studies, RBC obtained after HD were incubated in pre-dialysis plasma and NHE activity was measured thereafter. No change in NHE activity and a significant increase (p < 0.001) in GSH concentration in RBC were noted after HD with a glucose-containing fluid. HD with a glucose-free fluid resulted in a signi.cant decrease in NHE activity (p < 0.001) and GSH concentration (p < 0.001) in RBC. NHE activity (p < 0.001) and GSH concentration (p < 0.05) after HD were found to depend on the presence of glucose in the dialysis fluid. A positive correlation between GSH concentration and NHE activity after HD was found (p < 0.05). NHE activity after incubation of post-dialysis RBC in pre-dialysis plasma did not change in patients dialyzed with glucose and increased to pre-dialysis values in patients dialyzed with a glucose-free fluid. Conclusion: Decreased NHE activity in RBC after glucose-free HD is accompanied by decreased GSH concentration caused by lack of glucose in the dialysis fluid.

K e y w o r d s : sodium-proton exchanger – erythrocyte – haemodialysis – oxidative stress – chronic renal failure – cyclosporine A – uremic toxins.

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