The role of HO-1 in attenuating complement-dependent injury also needs to be addressed in glomerulopathies developed as a result of hyperactivation of the alternative complement pathway, as exemplified in C3 glomerulopathy, a heterogeneous disease entity in which abnormal control of complement activation via the AP results in predominant C3 fragment deposition within the glomerulus [111], aHUS, and IgA nephropathy. Here, HMOX1 is linked to IgA glomerulonephritis.