Rapidly progressive glomerulonephritis classification: Difference between revisions
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===Type III=== | ===Type III=== | ||
* Type III RPGN is also known as pauci immune RPGN. | * Type III RPGN is also known as pauci immune RPGN<ref name="robbins" />. | ||
* There are no anti [[GBM]] antibodies or no [[Immune complex|immune complexes]] involved. | * There are no anti [[GBM]] antibodies or no [[Immune complex|immune complexes]] involved. | ||
* It occurs due to the activation of [[Neutrophil|neutrophils]] in the GBM which is caused by the presence of [[Anti-neutrophil cytoplasmic antibody|ANCA]](p-ANCA or c-ANCA). | * It occurs due to the activation of [[Neutrophil|neutrophils]] in the GBM which is caused by the presence of [[Anti-neutrophil cytoplasmic antibody|ANCA]](p-ANCA or c-ANCA). | ||
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** Renal-limited necrotizing crescentic glomerulonephritis (NCGN) | ** Renal-limited necrotizing crescentic glomerulonephritis (NCGN) | ||
** [[Langerhans cell histiocytosis|Eosinophilic granulomatosis]] with polyangiitis (EGPA; Churg-Strauss syndrome) | ** [[Langerhans cell histiocytosis|Eosinophilic granulomatosis]] with polyangiitis (EGPA; Churg-Strauss syndrome) | ||
==References== | ==References== | ||
Revision as of 17:00, 18 July 2018
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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 .[1][2].
Type I
- Type I RPGN is characterized by the presence of autoantibodies directed against the glomerular basement membrane (GBM)[3].
- Type I also known as anti-GBM glomerulonephritis.
- The antibodies formed are known as anticollagen antibodies and react against type IV collagen of GBM.[4]
- 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)
- Connective tissue disorders
- Lupus nephritis
- Henoch-Schönlein purpural)
- Immunoglobulin A nephropathy
- Mixed cryoglobulinemia
- Membranoproliferative glomerulonephritis
Type III
- Type III RPGN is also known as pauci immune RPGN[4].
- 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)
References
- ↑ Couser WG (1988). "Rapidly progressive glomerulonephritis: classification, pathogenetic mechanisms, and therapy". Am J Kidney Dis. 11 (6): 449–64. PMID 3287904.
- ↑ Couser WG (1998). "Pathogenesis of glomerular damage in glomerulonephritis". Nephrol Dial Transplant. 13 Suppl 1: 10–5. PMID 9507491.
- ↑ Heeringa P, Brouwer E, Klok PA, Huitema MG, van den Born J, Weening JJ; et al. (1996). "Autoantibodies to myeloperoxidase aggravate mild anti-glomerular-basement-membrane-mediated glomerular injury in the rat". Am J Pathol. 149 (5): 1695–706. PMC 1865281. PMID 8909258.
- ↑ 4.0 4.1 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.