C4A and acute kidney tubular necrosis: The deposition of C3 and C4 is well established in glomerular disease, but only C3 deposition, and no evidence for C4 deposition, along tubules could be found in acute tubular necrosis after renal ischemia/reperfusion injury, indicating that the alternative pathway is the predominant complement activation pathway for the development of acute tubular necrosis [118].