C4 glomerulopathy historical perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Ali Poyan Mehr, M.D. [2]; Associate Editor(s)-in-Chief: Olufunmilola Olubukola M.D.[3]

Overview

There is limited information about the historical perspective of C4 glomerulopathy.

Historical Perspective

Sethi and Fervenza introduced a new classification based on immunofluorescence results for complement and immunoglobulin deposition. The deposition could either be by dysregulation of the complement alternative pathway or by immune complexes such as C4 glomerulopathy. The morphological, phenotypic characteristics of C4 glomerulopathy may be either those categorized by dense osmiophilic deposits or those of C4 glomerulonephritis, which displays isolated deposits. C4NeF was noticed in systemic lupus erythematosus, acute glomerulonephritis, and chronic proliferative glomerulonephritis and was also described in 100 hypocomplementemias MPGN patients with or without C3NeF. Sethi et al. defined C4d+ dominant Dense deposit disease wherein C3 was absent^[1]^[2]^[3]^[4]^[5].

References

↑ Sethi S, Fervenza FC (2012). “Membranoproliferative glomerulonephritis–a new look at an old entity”. N Engl J Med. 366 (12): 1119–31. doi:10.1056/NEJMra1108178. PMID 22435371.
↑ Halbwachs L, Leveillé M, Lesavre P, Wattel S, Leibowitch J (1980). “Nephritic factor of the classical pathway of complement: immunoglobulin G autoantibody directed against the classical pathway C3 convetase enzyme”. J Clin Invest. 65 (6): 1249–56. doi:10.1172/jci109787. PMC 371461. PMID 6902727.
↑ Ohi H, Yasugi T (1994). “Occurrence of C3 nephritic factor and C4 nephritic factor in membranoproliferative glomerulonephritis (MPGN)”. Clin Exp Immunol. 95 (2): 316–21. doi:10.1111/j.1365-2249.1994.tb06530.x. PMC 1534915. PMID 8306508.
↑ Tanuma Y, Ohi H, Watanabe S, Seki M, Hatano M (1989). “C3 nephritic factor and C4 nephritic factor in the serum of two patients with hypocomplementaemic membranoproliferative glomerulonephritis”. Clin Exp Immunol. 76 (1): 82–5. PMC 1541731. PMID 2736802.
↑ Daha MR, van Es LA (1980). “Relative resistance of the F-42-stabilized classical pathway C3 convertase to inactivation by C4-binding protein”. J Immunol. 125 (5): 2051–4. PMID 6903579.

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[pmid22435371-1] Sethi S, Fervenza FC (2012). “Membranoproliferative glomerulonephritis–a new look at an old entity”. N Engl J Med. 366 (12): 1119–31. doi:10.1056/NEJMra1108178. PMID 22435371.

[pmid6902727-2] Halbwachs L, Leveillé M, Lesavre P, Wattel S, Leibowitch J (1980). “Nephritic factor of the classical pathway of complement: immunoglobulin G autoantibody directed against the classical pathway C3 convetase enzyme”. J Clin Invest. 65 (6): 1249–56. doi:10.1172/jci109787. PMC 371461. PMID 6902727.

[pmid8306508-3] Ohi H, Yasugi T (1994). “Occurrence of C3 nephritic factor and C4 nephritic factor in membranoproliferative glomerulonephritis (MPGN)”. Clin Exp Immunol. 95 (2): 316–21. doi:10.1111/j.1365-2249.1994.tb06530.x. PMC 1534915. PMID 8306508.

[pmid2736802-4] Tanuma Y, Ohi H, Watanabe S, Seki M, Hatano M (1989). “C3 nephritic factor and C4 nephritic factor in the serum of two patients with hypocomplementaemic membranoproliferative glomerulonephritis”. Clin Exp Immunol. 76 (1): 82–5. PMC 1541731. PMID 2736802.

[pmid6903579-5] Daha MR, van Es LA (1980). “Relative resistance of the F-42-stabilized classical pathway C3 convertase to inactivation by C4-binding protein”. J Immunol. 125 (5): 2051–4. PMID 6903579.

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