Glomerular Diseases Dependent on Complement Activation, Including Atypical Hemolytic Uremic Syndrome, Membranoproliferative Glomerulonephritis, and C3 Glomerulopathy: Core Curriculum 2015

Complement is part of the innate immune system and plays a fundamental role in the clearance of immune complexes and cell debris. The main effector mechanisms of complement activation are induction of inflammatory response and phagocytosis and cell lysis. However, complement activation is a double-edged sword and has the potential to damage self-tissues. In order to avoid self-damage, there is an absolute need for strict control by fluid-phase and membrane-bound regulatory proteins. Thus, an underperforming regulatory system (due to either genetic or acquired abnormalities) can shift the balance between regulation and activation toward the latter and lead to tissue injury in response to otherwise innocuous stimuli.