Long-term erythropoietin therapy does not affect endothelial markers, coagulation activation and oxidative stress in haemodialyzed patients.

摘要

INTRODUCTION: Although the general improvement caused by recombinant human erythropoietin (rHuEPO) in the correction of uraemic anaemia cannot be questioned, some data suggest that the changes in the haemostasis, endothelial function and oxidative stress (SOX) are induced. The aim of the present study was to investigate the effect of one-year rHuEPO therapy on the coagulation activation, endothelial injury markers and SOX in haemodialysis (HD) patients. MATERIALS AND METHODS: Assessment of coagulation activation pathway: tissue factor (TF), its inhibitor (TFPI) and prothrombin fragment 1+2 (F1+2); endothelial injury markers: von Willebrand factor antigen (vWF:Ag) and thrombomodulin (TM); and several parameters related to SOX: total peroxide, Cu/Zn superoxide dismutase (Cu/Zn SOD) and autoantibodies to oxidized LDL (OxLDL-Ab) levels were performed in stable HD patients, treated for 12 months with rHuEPO (n=18; mean dose 113.5+/-41 U/kg/week) or not (with Hg<10 g/dl, n=8 and with Hg>10 g/dl, n=12), none of them on iron therapy. RESULTS: Patients with Hg<10 g/dl had a significantly lower erythrocytes count, Ht and Hg levels than those with Hg>10 g/dl and those on rHuEPO therapy. Long-term rHuEPO therapy does not affect coagulation pathway and SOX markers. Treatment with this hormone resulted in a tendency to decrease TM and vWF:Ag concentrations, however these changes did not reach a statistical significance. CONCLUSIONS: These results suggest that one-year rHuEPO therapy seems to exert no additional influence on coagulation activation, endothelial cell damage/activation markers and oxidative stress in patients undergoing regular HD in the absence of concomitant iron supplementation and irrespective from haemoglobin levels.