Hepatitis C virus (HCV) infection occurs frequently among haemodialysis (HD) patients and increases the risk of atherosclerosis. CD40 and Fas belong to tumor necrosis factor receptor (TNFR) superfamily, which play a role in hepatocyte apoptosis during HCV infection. The aim of the present study was to determine whether anti-HCV-seropositivity constitutes an additional risk factor for endothelial dysfunction in HD patients, and whether sCD40 and sFas could be associated with endothelial dysfunction.A total of 69 stable HD patients and 28 healthy controls were included in this study. Patients were divided into anti-HCV-seropositive (HCV[+], n=18) and anti-HCV- seronegative (HCV[-], n=51). The plasma endothelial markers: von Willebrand factor (vWF), thrombomodulin (TM), soluble adhesion molecules – sICAM-1, sVCAM-1 and TNFRs were assayed.HD patients showed a significant increase in the levels of TM, sVCAM-1, sCD40 and sFas compared to controls, and all these parameters were higher in HCV[+] than in HCV[-] patients. sICAM-1 concentrations were higher in the HCV[+] group compared to controls and the HCV[-] group. vWF levels were higher in HD patients than in the controls, however there was no difference in this parameter between HCV[+] and HCV[-] group. The anti-HCV-seropositivity and sCD40 were determined as an independent variables of TM, whereas anti-HCV-seropositivity and sFas were found as independent determinants of sICAM-1 and sVCAM-1 levels.This study showed that anti-HCV-seropositivity and TNF superfamily receptors: sCD40 and sFas are the novel determinants of the increased plasma endothelial dysfunction markers in haemodialysis patients.