Rapidly progressive glomerulonephritis classification: Difference between revisions
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==Overview== | ==Overview== | ||
Rapidly progressive glomerulonephritis is classified on the basis of cause of [[Glomerulus|glomerular]] injury.The [[Immunofluorescence|immunoflourescent microspcopic]] findings are used in determining the cause of glomerular injury. | |||
==Classification== | ==Classification== | ||
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===Type I=== | ===Type I=== | ||
* Type I RPGN is characterized by the presence of [[autoantibodies]] directed against the [[glomerular basement membrane]] (GBM)<ref name="pmid8909258">{{cite journal| author=Heeringa P, Brouwer E, Klok PA, Huitema MG, van den Born J, Weening JJ et al.| title=Autoantibodies to myeloperoxidase aggravate mild anti-glomerular-basement-membrane-mediated glomerular injury in the rat. | journal=Am J Pathol | year= 1996 | volume= 149 | issue= 5 | pages= 1695-706 | pmid=8909258 | doi= | pmc=1865281 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8909258 }} </ref>. | * Type I RPGN is characterized by the presence of [[autoantibodies]] directed against the [[glomerular basement membrane]] (GBM)<ref name="pmid8909258">{{cite journal| author=Heeringa P, Brouwer E, Klok PA, Huitema MG, van den Born J, Weening JJ et al.| title=Autoantibodies to myeloperoxidase aggravate mild anti-glomerular-basement-membrane-mediated glomerular injury in the rat. | journal=Am J Pathol | year= 1996 | volume= 149 | issue= 5 | pages= 1695-706 | pmid=8909258 | doi= | pmc=1865281 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8909258 }} </ref>. | ||
* Type I also known as anti-[[GBM]] glomerulonephritis. | * Type I also known as anti-[[GBM]] [[Glomerular disease|glomerulonephritis.]] | ||
* The antibodies formed are known as anticollagen antibodies and react against type IV [[collagen]] of [[GBM]].<ref name="robbins">{{cite book |author=Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. |title=Robbins and Cotran pathologic basis of disease |publisher=Elsevier Saunders |location=St. Louis, MO |year=2005 |pages=pp976-8 |isbn=0-7216-0187-1 |oclc= |doi=}}</ref> | * The antibodies formed are known as anticollagen antibodies and react against type IV [[collagen]] of [[GBM]].<ref name="robbins">{{cite book |author=Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. |title=Robbins and Cotran pathologic basis of disease |publisher=Elsevier Saunders |location=St. Louis, MO |year=2005 |pages=pp976-8 |isbn=0-7216-0187-1 |oclc= |doi=}}</ref> | ||
* The antibodies can be produced by a stimulus such as viral [[Upper respiratory tract infection|URTI]] that exposes alveolar collagen membrane or it can be idiopathic. | * The antibodies can be produced by a stimulus such as viral [[Upper respiratory tract infection|URTI]] that exposes [[Alveolus|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]]. | * The antibodies formed can act against alveolar membrane and lungs get involved in some cases such as in [[goodpasture syndrome]]. | ||
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* [[Connective tissue disease|Connective tissue disorders]] | * [[Connective tissue disease|Connective tissue disorders]] | ||
* [[Lupus nephritis]] | * [[Lupus nephritis]] | ||
* [[Henoch-Schönlein purpura|Henoch-Schönlein | * [[Henoch-Schönlein purpura|Henoch-Schönlein purpura]] | ||
* [[IgA nephropathy|Immunoglobulin A nephropathy]] | * [[IgA nephropathy|Immunoglobulin A nephropathy]] | ||
* Mixed [[cryoglobulinemia]] | * Mixed [[cryoglobulinemia]] | ||
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* 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 is further classified into 2 types: | * It is further classified into 2 types: | ||
** Immunogenic - ANCA positive | ** Immunogenic - [[Anti-neutrophil cytoplasmic antibody|ANCA]] positive | ||
** Non immunogenic- ANCA negative/ Idiopathic | ** Non immunogenic- ANCA negative/ Idiopathic | ||
* ANCAs cause the release of lytic enzymes from neutrophils that damage the GBM. | * ANCAs cause the release of lytic enzymes from [[Neutrophil|neutrophils]] that damage the GBM. | ||
* Systemic [[vasculitis]] is present in most of the cases but some occur without systemic involvement and only renal findings maybe present. | * Systemic [[vasculitis]] is present in most of the cases but some occur without systemic involvement and only renal findings maybe present. | ||
* Examples include | * Examples include | ||
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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) | ||
** Drugs- hydralazine, allopurinol and rifampin. | ** Drugs- [[hydralazine]], [[allopurinol]] and [[rifampin]]. | ||
==References== | ==References== | ||
Revision as of 16:13, 23 July 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Rapidly progressive glomerulonephritis is classified on the basis of cause of glomerular injury.The immunoflourescent microspcopic findings are used in determining the cause of glomerular injury.
Classification
RPGN is classified on the basis of the cause of glomerular injury and the findings from light and immunofluorescence microscopy.[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 purpura
- 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 is further classified into 2 types:
- Immunogenic - ANCA positive
- Non immunogenic- ANCA negative/ Idiopathic
- ANCAs cause the release of lytic enzymes from neutrophils that damage the GBM.
- 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)
- Drugs- hydralazine, allopurinol and rifampin.
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.