Rapidly progressive glomerulonephritis classification
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Classification
RPGN is classified on the basis of the cause of crescent formation resulting from glomerular injury.
Type I
- Type I RPGN is characterized by the presence of autoantibodies directed against the glomerular basement membrane (GBM).
- Type I also known as anti-GBM glomerulonephritis.
- The antibodies formed are known as anticollagen antibodies and react against type IV collagen of GBM.[1]
- The antibodies can be produced by a stimulus such as viral URTI that exposes alveolar collagen membrane or it can be idiopathic.
- The antibodies formed can act against alveolar membrane and lungs get involved in some cases such as in goodpasture syndrome.
Type II
- Type II RPGN is caused by the deposition of immune complexes in the GBM.
- Immune complexes can be formed in certain infections or in connective tissue disorders.
- These immune complexes deposit over the GBM and activate the complement system resulting in crescent formation.
- Examples include postinfectious (staphylococci/streptococci), collagen-vascular disease, lupus nephritis, Henoch-Schönlein purpural), immunoglobulin A nephropats), mixed cryoglobulinemia, primary renal disease, membranoproliferative glomerulonephritis, fibrillary glomerulonephritis.
Type III
- Type III RPGN is also known as pauci immune RPGN.
- There are no anti GBM antibodies or no immune complexes involved.
- It occurs due to the activation of neutrophils in the GBM which is caused by the presence of ANCA(p-ANCA or c-ANCA).
- Systemic vasculitis is present in most of the cases but some occur without systemic involvement and only renal findings maybe present.
- Examples include Granulomatosis with polyangiitis (Wegener granulomatosis)
- Microscopic polyangiitis (MPA)
- Renal-limited necrotizing crescentic glomerulonephritis (NCGN)
- Eosinophilic granulomatosis with polyangiitis (EGPA; Churg-Strauss syndrome)
- Examples include Granulomatosis with polyangiitis (Wegener granulomatosis)
.[1]
References
- ↑ 1.0 1.1 Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease. St. Louis, MO: Elsevier Saunders. pp. pp976–8. ISBN 0-7216-0187-1.