Pathogenesis of Membranoproliferative glomerulonephritis

What is the Pathogenesis of Membranoproliferative glomerulonephritis?

In primary forms of Membranoproliferative glomerulonephritis, the mechanism of disease centers on abnormal activation of the complement cascade.

There are three distinct patterns of complement activation in the three types of Membranoproliferative glomerulonephritis.

• In type I disease, the process is initiated by immune complex deposition within the kidney and involvement of the classic pathway. The source of the immune complexes is unknown in the idiopathic form of the disease. Patients have low levels of C3, C4, C6, C7, and/or C9.

• In the type II variant, continuous overactivity of the complement cascade involves an amplification loop in the alternative pathway, characterized mainly by markedly depressed C3 levels. An IgG or IgM autoantibody, termed C3 nephritic factor, is present in the majority of patients with DDD.

• Type III Membranoproliferative glomerulonephritis appears to have features in common with type I disease as well as evidence of activation of the terminal complement pathway, with low levels of C3, C5, and properdin. In the secondary forms of Membranoproliferative glomerulonephritis, it is presumed that there is immune complex–mediated activation of the complement cascade.

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