CD55 and focal segmental glomerulosclerosis: Prior data also suggest that complement can activate in the glomeruli of FSGS patients through the alternative pathway as a consequence of the cleavage of the key complement regulator decay accelerating factor (CD55) on the membranes of injured podocytes.10 Therefore, it is possible that different mechanisms (IgM-mediated and IgM-independent) activate complement in FSGS, possibly in different phases of the disease.