Hepatitis C virus seropositivity and TNF superfamily receptors: sCD40, sFas--the new putative determinants of endothelial dysfunction in haemodialysis patients.

Introduction: 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.

Materials And Methods: 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.

Results: 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.

Conclusions: 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.