Rapidly progressive glomerulonephritis causes: Difference between revisions
Esther Lee (talk | contribs) (Created page with "__NOTOC__ {{Rapidly progressive glomerulonephritis}} Please help WikiDoc by adding content here. It's easy! Click here to learn about editing....") |
No edit summary |
||
| Line 1: | Line 1: | ||
__NOTOC__ | __NOTOC__ | ||
{{Rapidly progressive glomerulonephritis}} | {{Rapidly progressive glomerulonephritis}} | ||
{{CMG}} | |||
==Overview== | |||
==Causes== | |||
===Primary RPGN=== | |||
RPGN may be a primary condition. The diagnosis of primary glomerulonephritis is made when the clinical syndrome of the disease complies with the new classification of RPGN based on the 5 types of disease. | |||
Nonetheless, ruling out other causes of RPGN is necessary before the diagnosis of primary RPGN is made. | |||
The cause of ANCA levels in patients with ANCA-associated glomerulonephritis is not known. Environmental and genetic factors have been postulated. It is believed that infectious etiologies, such as arboviruses, may be contributory. These findings are based only on observations and small studies that patients with ANCA-associated glomerulonephritis are more commonly diagnosed during “flu season”, flu-like prodrome is usually the most common presenting symptoms of these patients, and presence of serological proof of previous arbovirus infection. Further disease progression in ANCA-associated diseases into clinical syndromes of polyarteritis nodosa and Wegener granulomatosis has been postulated to be caused by activation of autoantibody-induced leukocytes.<ref name="pmid2221646">{{cite journal| author=Falk RJ, Hogan S, Carey TS, Jennette JC| title=Clinical course of anti-neutrophil cytoplasmic autoantibody-associated glomerulonephritis and systemic vasculitis. The Glomerular Disease Collaborative Network. | journal=Ann Intern Med | year= 1990 | volume= 113 | issue= 9 | pages= 656-63 | pmid=2221646 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2221646 }} </ref> However, no consistent validation of such claims has been made. | |||
===Secondary RPGN=== | |||
====Infections==== | |||
*Infective endocarditis | |||
*Sepsis | |||
*HBV infection with vasculitis or cryoglobulinemia | |||
*HCV infection with vasculitis or cryoglobulinemia | |||
====Drugs==== | |||
*Allopurinol | |||
*D-penicillamine | |||
*Hydralazine | |||
*Rifampin | |||
====Multi-Organ Disease==== | |||
*Systemic lupus erythematosus | |||
*Henoch-Schonlein purpura | |||
*Systemic necrotizing vasculitis | |||
*Relapsing polychondritis | |||
*Cryoglobulinemia | |||
*Other vasculitides | |||
====Malignancies==== | |||
*Colon cancer | |||
*Pulmonary cancer | |||
*Lymphoma | |||
====Other Conditions==== | |||
*Behcet’s disease | |||
*Membranoproliferative glomerulonephritis | |||
*IgA nephropathy | |||
*Poststreptococcal glomerulonephritis | |||
*Hereditary nephritis | |||
==References== | ==References== | ||
Revision as of 19:28, 8 May 2018
|
Rapidly progressive glomerulonephritis Microchapters |
|
Differentiating Rapidly progressive glomerulonephritis from other Diseases |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Rapidly progressive glomerulonephritis causes On the Web |
|
American Roentgen Ray Society Images of Rapidly progressive glomerulonephritis causes |
|
Directions to Hospitals Treating Rapidly progressive glomerulonephritis |
|
Risk calculators and risk factors for Rapidly progressive glomerulonephritis causes |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Causes
Primary RPGN
RPGN may be a primary condition. The diagnosis of primary glomerulonephritis is made when the clinical syndrome of the disease complies with the new classification of RPGN based on the 5 types of disease. Nonetheless, ruling out other causes of RPGN is necessary before the diagnosis of primary RPGN is made.
The cause of ANCA levels in patients with ANCA-associated glomerulonephritis is not known. Environmental and genetic factors have been postulated. It is believed that infectious etiologies, such as arboviruses, may be contributory. These findings are based only on observations and small studies that patients with ANCA-associated glomerulonephritis are more commonly diagnosed during “flu season”, flu-like prodrome is usually the most common presenting symptoms of these patients, and presence of serological proof of previous arbovirus infection. Further disease progression in ANCA-associated diseases into clinical syndromes of polyarteritis nodosa and Wegener granulomatosis has been postulated to be caused by activation of autoantibody-induced leukocytes.[1] However, no consistent validation of such claims has been made.
Secondary RPGN
Infections
- Infective endocarditis
- Sepsis
- HBV infection with vasculitis or cryoglobulinemia
- HCV infection with vasculitis or cryoglobulinemia
Drugs
- Allopurinol
- D-penicillamine
- Hydralazine
- Rifampin
Multi-Organ Disease
- Systemic lupus erythematosus
- Henoch-Schonlein purpura
- Systemic necrotizing vasculitis
- Relapsing polychondritis
- Cryoglobulinemia
- Other vasculitides
Malignancies
- Colon cancer
- Pulmonary cancer
- Lymphoma
Other Conditions
- Behcet’s disease
- Membranoproliferative glomerulonephritis
- IgA nephropathy
- Poststreptococcal glomerulonephritis
- Hereditary nephritis
References
- ↑ Falk RJ, Hogan S, Carey TS, Jennette JC (1990). "Clinical course of anti-neutrophil cytoplasmic autoantibody-associated glomerulonephritis and systemic vasculitis. The Glomerular Disease Collaborative Network". Ann Intern Med. 113 (9): 656–63. PMID 2221646.