Sepsis results from activation to complement cascade, an appropriate and necessary response to infection. Some studies have demonstrated that CHDF could be an effective therapy for removing inflammatory cytokines for systemic inflammatory response syndrome (SIRS). The aim of this study is to evaluate the changes in the complement cascade during CHDF and to determine the effect of CHDF on sepsis.

Ten patients with sepsis underwent CHDF for at least 3 days in our ICU. Patients with chronic renal failure or receiving steroid therapy were excluded. We assessed complement function and concentrations or activities of CH50, C1q, C3a, C3-proactivator, C3, C4, albumin and C-reactive protein (CRP). Blood samples were obtained from an arterial catheter before and 3 days after the start of CHDF. Blood samples from both membrane sites and the CHDF filtrate were obtained at 2, 6 and 12 hours after the start of CHDF. Statistical analysis was performed on the changes during CHDF and both sites of the membrane (P < 0.05).

Six patients survived (S-group) and four patients did not survive (N-group). Levels of C3a before CHDF were extremely high and decreased significantly during CHDF in survived group. The levels of CH50 and C3 before CHDF were low, but did not change significantly during CHDF. The levels of C1q, C4, and C3 pro-activator were within their normal ranges, and did not change during this study. CH50 and C3a were detected in CHDF filtrate. Only the levels of C3a increased significantly through the dialysis membrane.

It was thought that high levels of C3a indicated activation of the complement cascade and low levels of CH50 and C3 occurred due to consumption during sepsis. CHDF can be an effective therapy for sepsis because C3a (chemotactic factor) decreased significantly during CHDF. The complement cascade except for C3a did not change during CHDF in this study. However CHDF may have the potential to activate the complement cascade because the levels of C3a increased through the dialysis membrane.