Rapidly progressive glomerulonephritis classification: Difference between revisions
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==Classification== | ==Classification== | ||
Based on the type of 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 is also known as anti-GBM glomerulonephritis. | |||
In addition to the anti-GBM antibodies, some cases of type I RPGN are also associated with antibodies directed against the [[basement membrane]] of lung [[alveoli]], producing [[Goodpasture syndrome]]. The majority of type I disease, however, features anti-GBM antibodies alone; these cases are considered idiopathic.<ref name="robbins"/> | * Antibodies are directed against a particular protein found in the GBM, [[type IV collagen]], specifically the noncollagenous region of its α<sub>3</sub> chain.<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> | ||
** In addition to the anti-GBM antibodies, some cases of type I RPGN are also associated with antibodies directed against the [[basement membrane]] of lung [[alveoli]], producing [[Goodpasture syndrome]]. The majority of type I disease, however, features anti-GBM antibodies alone; these cases are considered idiopathic.<ref name="robbins" /> | |||
===Type II=== | ===Type II=== | ||
RPGN caused by the deposition of [[immune complex]]es accounts for 25% of RPGN and is classified as type II. Thus any [[immune complex disease]] that involves the glomerulus may progress to RPGN if severe enough. These diseases include [[systemic lupus erythematosus]], [[postinfectious glomerulonephritis]], [[Henoch-Schönlein purpura]], and [[IgA nephropathy]].<ref name="robbins"/> | * RPGN caused by the deposition of [[immune complex]]es accounts for 25% of RPGN and is classified as type II. Thus any [[immune complex disease]] that involves the glomerulus may progress to RPGN if severe enough. These diseases include [[systemic lupus erythematosus]], [[postinfectious glomerulonephritis]], [[Henoch-Schönlein purpura]], and [[IgA nephropathy]].<ref name="robbins" /> | ||
===Type III=== | ===Type III=== | ||
Also known as pauci-immune RPGN, type III RPGN accounts for 55% of RPGN and features neither immune complex deposition nor anti-GBM antibodies. Instead, the glomeruli are damaged in an undefined manner, perhaps through the activation of [[neutrophil]]s in response to [[anti-neutrophil cytoplasmic antibodies]] (ANCA). Type III RPGN may be isolated to the glomerulus (primary, or idiopathic) or associated with a systemic disease (secondary). In most cases of the latter, the systemic disease is an ANCA-associated [[vasculitis]] such as [[Wegener granulomatosis]], [[microscopic polyangiitis]], or [[Churg-Strauss syndrome]].<ref name="robbins"/> | * Also known as pauci-immune RPGN, type III RPGN accounts for 55% of RPGN and features neither immune complex deposition nor anti-GBM antibodies. Instead, the glomeruli are damaged in an undefined manner, perhaps through the activation of [[neutrophil]]s in response to [[anti-neutrophil cytoplasmic antibodies]] (ANCA). Type III RPGN may be isolated to the glomerulus (primary, or idiopathic) or associated with a systemic disease (secondary). In most cases of the latter, the systemic disease is an ANCA-associated [[vasculitis]] such as [[Wegener granulomatosis]], [[microscopic polyangiitis]], or [[Churg-Strauss syndrome]].<ref name="robbins" /> | ||
Classification of type III RPGN into primary or secondary may be unnecessary, as primary type III RPGN and secondary type III RPGN may represent a spectrum of the same disease process.<ref name="robbins" /> | |||
Classification of type III RPGN into primary or secondary may be unnecessary, as primary type III RPGN and secondary type III RPGN may represent a spectrum of the same disease process.<ref name="robbins"/> | |||
==References== | ==References== | ||
Revision as of 22:44, 17 July 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Classification
Based on the type of glomerular injury
Type I
- Type I RPGN is characterized by the presence of autoantibodies directed against the glomerular basement membrane (GBM).
- Type I is also known as anti-GBM glomerulonephritis.
- Antibodies are directed against a particular protein found in the GBM, type IV collagen, specifically the noncollagenous region of its α3 chain.[1]
- In addition to the anti-GBM antibodies, some cases of type I RPGN are also associated with antibodies directed against the basement membrane of lung alveoli, producing Goodpasture syndrome. The majority of type I disease, however, features anti-GBM antibodies alone; these cases are considered idiopathic.[1]
Type II
- RPGN caused by the deposition of immune complexes accounts for 25% of RPGN and is classified as type II. Thus any immune complex disease that involves the glomerulus may progress to RPGN if severe enough. These diseases include systemic lupus erythematosus, postinfectious glomerulonephritis, Henoch-Schönlein purpura, and IgA nephropathy.[1]
Type III
- Also known as pauci-immune RPGN, type III RPGN accounts for 55% of RPGN and features neither immune complex deposition nor anti-GBM antibodies. Instead, the glomeruli are damaged in an undefined manner, perhaps through the activation of neutrophils in response to anti-neutrophil cytoplasmic antibodies (ANCA). Type III RPGN may be isolated to the glomerulus (primary, or idiopathic) or associated with a systemic disease (secondary). In most cases of the latter, the systemic disease is an ANCA-associated vasculitis such as Wegener granulomatosis, microscopic polyangiitis, or Churg-Strauss syndrome.[1]
Classification of type III RPGN into primary or secondary may be unnecessary, as primary type III RPGN and secondary type III RPGN may represent a spectrum of the same disease process.[1]