Abstract
Hepatitis C Virus (HCV) infection remains prevalent in patients receiving regular dialysis all over the world. The adverse impact of anti-HCV serologic status on mortality in the dialysis population has been documented. Antiviral therapy for hepatitis C in chronic kidney disease (CKD) patients, including the dialysis population, is still unsatisfactory. Several findings support a different course of HCV in dialysis patients versus the non-uremic population. The HCV viral load appears lower in hemodialysis patients with HCV despite the immune compromise caused by chronic uremia; the histologic abnormalities seem milder, and a severe clinical course of chronic hepatitis C is unusual in most hemodialysis (HD) patients. It appears that the HD procedure per se can preserve patients from an aggressive course of HCV by reducing the viral load (HCV RNA). The mechanisms by which the HD procedure lowers HCV viremia remain largely speculative: the passage of viral particles into the dialysate, the trapping of the virus on the surface of the dialyzer membrane, and an indirect host-mediated mechanism have been cited. The latter hypothesis implicates the production of interferon-alpha, hepatocyte growth factor, or other cytokines provided with antiviral activities during the hemodialysis sessions. Clinical trials aimed at clarifying this issue are under way.
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