During clinical hemodialysis, interactions between blood and dialysis membranes lead to the activation of several pathways such as the coagulation, kallikrein and complement pathways. The sum of these interactions defines the biocompatibility of the dialysis membrane; Cuprophane membranes, the most widely used dialysis membranes elicit intense blood-membrane interactions. Complement activation can be measured by determining the concentration of the activated third and fifth component of the complement cascade, namely C3a and C5a. These active products lead to the well known neutropenia seen during the early phase of dialysis. However, the neutropenia is only the most visible manifestation of the effects of complement activation. C5a-induced secretion of granule enzymes from neutrophils and their subsequent desensitization to further chemotaxis and phagocytosis may be an important factor in the incidence of infections in the dialysis patient. Endothelial cell damage by complement stimulated granulocytes mediated via superoxide anion may also play a role in the pulmonary dysfunction seen in dialysis patients, and recent evidence suggests that complement products may lead to cardiac dysfunction manifested by impaired ventricular contractility. Although some of these events may not be mediated directly by activated complement products, recent studies suggest that they play a role in the activation of several other pathways and pathophysiological process.