Rapidly progressive glomerulonephritis classification: Difference between revisions
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==Classification== | ==Classification== | ||
RPGN is classified on the basis of the cause of crescent formation resulting from glomerular injury | RPGN is classified on the basis of the cause of crescent formation resulting from glomerular injury | ||
===Type I=== | ===Type I=== | ||
* Type I RPGN is characterized by the presence of [[autoantibodies]] directed against the [[glomerular basement membrane]] (GBM). | * 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. | * Type I also known as anti-[[GBM]] 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 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 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]]. | ||
===Type II=== | ===Type II=== | ||
* Type II RPGN is caused by the deposition of immune complexes in the GBM. | * Type II RPGN is caused by the deposition of [[Immune complex|immune complexes]] in the [[GBM|GBM.]] | ||
* Immune complexes can be formed in certain infections or in connective tissue disorders. | * Immune complexes can be formed in certain infections or in [[Connective tissue disease|connective tissue disorders.]] | ||
* These immune complexes deposit over the GBM and activate the complement system resulting in crescent formation. | * These immune complexes deposit over the GBM and activate the [[complement system]] resulting in [[Crescent Rising|crescent]] formation. | ||
* Examples include | * Examples include: | ||
* Postinfectious ([[Staphylococcus aureus|staphylococci]]/[[Streptococcus|streptococci]]) | |||
* [[Connective tissue disease|Connective tissue disorders]] | |||
* [[Lupus nephritis]] | |||
* [[Henoch-Schönlein purpura|Henoch-Schönlein purpural]]) | |||
* [[IgA nephropathy|Immunoglobulin A nephropathy]] | |||
* Mixed [[cryoglobulinemia]] | |||
* [[Membranoproliferative glomerulonephritis]] | |||
===Type III=== | ===Type III=== | ||
* Type III RPGN is also known as pauci immune RPGN. | * Type III RPGN is also known as pauci immune RPGN. | ||
* There are no anti GBM antibodies or no immune complexes involved. | * There are no anti [[GBM]] antibodies or no [[Immune complex|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). | * 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). | ||
* 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 | |||
** | ** [[Granulomatosis with polyangiitis]] (Wegener granulomatosis) | ||
** [[Microscopic polyangiitis]] (MPA) | |||
** | ** Renal-limited necrotizing crescentic glomerulonephritis (NCGN) | ||
** [[Langerhans cell histiocytosis|Eosinophilic granulomatosis]] with polyangiitis (EGPA; Churg-Strauss syndrome) | |||
.<ref name="robbins" /> | .<ref name="robbins" /> | ||
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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)
- 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.
- 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)
.[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.