Hepatitis C virus (HCV) infection remains frequent among dialysis patients. The relationship between viral load and liver disease progression is currently a matter of debate; however, low HCV viral load (HCV RNA) is a well established predictor of successful antiviral treatment. Dialysis patients have immune compromise due to uremia; in spite of this, HCV viral load is not high and does not increase over time. A number of studies support the notion that this dynamics of HCV viral load may be related to lowering of HCV RNA titers during the HD procedure. It has been suggested that the intradialytic reduction of HCV is membrane-dependent; polysulphone (PS) and hemophan membranes appear more effective. Various mechanisms have been mentioned to explain the reduction of HCV RNA during hemodialysis (HD): adsorption of HCV onto dialysis membrane, HCV escape into spent dialysate, destruction of HCV particles or increased interferon (IFN) activity. Several investigators have noted that, at the end of the HD procedure, a virological rebound of HCV viremia occurs. Some suggestions have been made to minimize the risk for HCV escape into spent dialysate. However, controversial evidence on these issues exists: the HCV RNA reduction during HD procedures has not been seen in some studies and the relationship between the intra-dialytic reduction of HCV RNA titers and dialysis membrane is not completely understood. It is evident that additional long-term longitudinal studies by serial viral load estimations are needed to better define the dynamics of HCV viral load in the dialysis population.