An update on glomerulopathies : etiology and pathogenesis by Sharma S Prabhakar

By Sharma S Prabhakar

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Circulating auto-antibodies are made up of the same he same IgG4/IgG1 isotypes indicating a good homology between the circulating and the renal counterparts (Figure 2). How the IgG isotype can influence pathogenesis of MGN is still matter of debate since a few issues are not clear. The first one is related to the described inability of IgG4 to activate complement, that might suggests an independence between IgG4 deposition and C5b-9 formation. Another concern is about IgG1: their role in MGN need to be re-evaluated.

Identified mutations affect the activity of complement proteins that are either part of the C3 convertase (C3 and factor B) or that are regulators (factor H, factor I, membrane cofactor protein, CFHR5) of complement activation. , 2009). Autoantibodies against the complement regulator factor H are detected in some patients with atypical hemolytic uremic syndrome and patients with dense deposit disease, and autoantibodies against the C3 convertase (C3 nephritic factor [C3NeF] or anti-factor B) in patients with MPGN, dense deposit disease and C3 glomerulonephritis.

On the other hand, the plasma regulator factor H, and the membrane proteins decay accelerating factor and complement receptor type 1 destabilize the convertase. In addition, the plasma serine protease factor I can cleave C3b in the presence of one of its cofactors (factor H, membrane cofactor protein, complement receptor type 1), and the inactivated C3b (iC3b) can no longer form a convertase (Figure 2). 34 An Update on Glomerulopathies – Etiology and Pathogenesis Fig. 2. Activation and regulation of the alternative pathway and the C3 convertase.

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An update on glomerulopathies : etiology and pathogenesis by Sharma S Prabhakar
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