Abstract
The serum complement profile of patients with systemic or discoid lupus erythematosus, synovitis, vasculitides, certain recurrent or chronic skin rashes, recurrent or fulminant infections, particularly with Neisseria, may reveal homozygous deficiencies of complement components causally related to the illness. The nephritis of systemic lupus erythematosus (SLE) is often accompanied by a distinctive complement profile which indicates classical pathway activation and which can be used as an index of the success of treatment. In membranoproliferative glomerulonephritis (MPGN), the hypocomplementemia may reflect classical pathway activation in type I, the nephritic factor of the amplification loop in type II, or a nephritic factor activating terminal components in type III. In acute poststreptococcal glomerulonephritis, the cause of the hypocomplementemia is not known but the profile usually differs from that of MPGN or SLE. In these acquired hypocomplementemias, the profile supplements the renal biopsy in providing diagnostic information.
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