Rapidly progressive glomerulonephritis risk factors: Difference between revisions

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{{Rapidly progressive glomerulonephritis}}
{{Rapidly progressive glomerulonephritis}}
{{CMG}}; {{AE}} {{JSS}}


==Overview==
==Overview==
Common risk factors in the development of rapidly progressive glomerulonephritis may be occupational, environmental, [[genetic]], and [[viral]]. However, we don't know what causes the antibodies to form.
Common risk factors in the development of rapidly progressive glomerulonephritis may be occupational, environmental, [[genetic]], and [[viral]].


==Risk Factors==
==Risk Factors==
Common risk factors in the development of rapidly progressive glomerulonephritis may be occupational, environmental, [[genetic]], and [[viral]]. <ref name="pmid24456936">{{cite journal| author=Hellmark T, Segelmark M| title=Diagnosis and classification of Goodpasture's disease (anti-GBM). | journal=J Autoimmun | year= 2014 | volume= 48-49 | issue=  | pages= 108-12 | pmid=24456936 | doi=10.1016/j.jaut.2014.01.024 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24456936  }} </ref><ref name="pmid1536151">{{cite journal| author=Bombassei GJ, Kaplan AA| title=The association between hydrocarbon exposure and anti-glomerular basement membrane antibody-mediated disease (Goodpasture's syndrome). | journal=Am J Ind Med | year= 1992 | volume= 21 | issue= 2 | pages= 141-53 | pmid=1536151 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1536151  }} </ref>
Common risk factors in the development of rapidly progressive glomerulonephritis may be occupational, environmental, [[genetic]], and [[viral]]. <ref name="pmid24456936">{{cite journal| author=Hellmark T, Segelmark M| title=Diagnosis and classification of Goodpasture's disease (anti-GBM). | journal=J Autoimmun | year= 2014 | volume= 48-49 | issue=  | pages= 108-12 | pmid=24456936 | doi=10.1016/j.jaut.2014.01.024 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24456936  }} </ref><ref name="pmid1536151">{{cite journal| author=Bombassei GJ, Kaplan AA| title=The association between hydrocarbon exposure and anti-glomerular basement membrane antibody-mediated disease (Goodpasture's syndrome). | journal=Am J Ind Med | year= 1992 | volume= 21 | issue= 2 | pages= 141-53 | pmid=1536151 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1536151  }} </ref>
*Recent studies suggest that infections such as [[viral]] or [[bacterial]] may play a role through [[molecular mimicry]] and increase the risk of developing rapidly progressive glomerulonephritis.
 
*Other factors that may increase the risk of rapidly progressive glomerulonephritis and early initiation of disease include [[behavioral]] and social factors.
=== Common risk factrors ===
**An example of environmental, [[genetic]], behavioral and social factors include [[smoking]], using [[cocaine]], being exposed to solvents such as [[formaldehyde]] and [[hydrocarbons]].
* Pre existing [[renal disease]].
**Genetically, the presence of allele HLA DRB1-1501 is strongly correlated to the disease.<ref name="pmid19741587">{{cite journal| author=Zhao J, Cui Z, Yang R, Jia XY, Zhang Y, Zhao MH| title=Anti-glomerular basement membrane autoantibodies against different target antigens are associated with disease severity. | journal=Kidney Int | year= 2009 | volume= 76 | issue= 10 | pages= 1108-15 | pmid=19741587 | doi=10.1038/ki.2009.348 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19741587  }} </ref>
 
**The allele HLA DRB1-1501 is present in over 80% of patients would Goodpasture syndrome.<ref name="pmid27049372">{{cite journal| author=Couser WG| title=Pathogenesis and treatment of glomerulonephritis-an update. | journal=J Bras Nefrol | year= 2016 | volume= 38 | issue= 1 | pages= 107-22 | pmid=27049372 | doi=10.5935/0101-2800.20160016 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27049372  }} </ref>
* Presence of [[HLA]]DRB1, HLA DP1, DQ and DRB4s<ref name="pmid15652778">{{cite journal| author=Jagiello P, Gross WL, Epplen JT| title=Complex genetics of Wegener granulomatosis. | journal=Autoimmun Rev | year= 2005 | volume= 4 | issue= 1 | pages= 42-7 | pmid=15652778 | doi=10.1016/j.autrev.2004.06.003 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15652778  }} </ref>
**It is also suggestive that the disease may be initiated following a [[viral]] or [[bacterial]] infection, however, there is no specific cause of why this occurs. Possible antigens such as that found in the [[influenza virus]] may play a role due to cross-reactivity in the [[basement membrane]].<ref name="pmid4571918">{{cite journal| author=Wilson CB, Dixon FJ| title=Anti-glomerular basement membrane antibody-induced glomerulonephritis. | journal=Kidney Int | year= 1973 | volume= 3 | issue= 2 | pages= 74-89 | pmid=4571918 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4571918  }}</ref>
 
*In addition, any of the following conditions may also increase [[antibody]] access to the [[alveolar]] and [[Glomerular basement membrane|glomerular basement membranes]]:
* [[Upper respiratory tract infection]]
**[[Upper respiratory infections]]
* [[Sepsis]]
**[[Septicemia]]
* Tobacco smoking
**Volatile [[hydrocarbons]]
* Intravenous drug abuse
**Increased capillary [[hydrostatic pressure]]
 
**Tobacco [[smoking]]
=== Less common risk factors ===
**High concentrations of [[FiO2]] (oxygen)
* Cocaine use
* Exposure to hydrocarbons( formaldehyde)
* HIgh concenteration of FiO<sub>2</sub>


==References==
==References==

Latest revision as of 19:32, 24 July 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Jogeet Singh Sekhon, M.D. [2]

Overview

Common risk factors in the development of rapidly progressive glomerulonephritis may be occupational, environmental, genetic, and viral.

Risk Factors

Common risk factors in the development of rapidly progressive glomerulonephritis may be occupational, environmental, genetic, and viral. [1][2]

Common risk factrors

  • Presence of HLADRB1, HLA DP1, DQ and DRB4s[3]

Less common risk factors

  • Cocaine use
  • Exposure to hydrocarbons( formaldehyde)
  • HIgh concenteration of FiO2

References

  1. Hellmark T, Segelmark M (2014). "Diagnosis and classification of Goodpasture's disease (anti-GBM)". J Autoimmun. 48-49: 108–12. doi:10.1016/j.jaut.2014.01.024. PMID 24456936.
  2. Bombassei GJ, Kaplan AA (1992). "The association between hydrocarbon exposure and anti-glomerular basement membrane antibody-mediated disease (Goodpasture's syndrome)". Am J Ind Med. 21 (2): 141–53. PMID 1536151.
  3. Jagiello P, Gross WL, Epplen JT (2005). "Complex genetics of Wegener granulomatosis". Autoimmun Rev. 4 (1): 42–7. doi:10.1016/j.autrev.2004.06.003. PMID 15652778.

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