Goodpasture syndrome risk factors
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Ali Poyan Mehr, M.D. [2]Associate Editor(s)-in-Chief: Krzysztof Wierzbicki M.D. [3]
Overview
Common risk factors in the development of Goodpasture syndrome may be occupational, environmental, genetic, and viral. However, we don’t known what causes the antibodies to form.
Risk Factors
Common risk factors in the development of Goodpasture syndrome may be occupational, environmental, genetic, and viral. [1][2]
- Recent studies suggest that infections such as viral or bacterial may play a role through molecular mimicry and increase the risk of developing Goodpasture syndrome.
- Other factors that may increase the risk of Goodpasture syndrome and early initiation of disease include behavioral and social factors.
- An example of environmental, genetic, behavioral and social factors include smoking, using cocaine, being exposed to solvents such as formaldehyde and hydrocarbons.
- Genetically, the presence of allele HLA DRB1-1501 is strongly correlated to the disease.[3]
- The allele HLA DRB1-1501 is present in over 80% of patients would Goodpasture syndrome.[4]
- 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.[5]
- In addition, any of the following conditions may also increase antibody access to the alveolar and glomerular basement membranes.
- Upper respiratory infections
- Septicemia
- Volatile hydrocarbons
- Increased capillary hydrostatic pressure
- Tobacco smoking
- High concentrations of FiO2 (oxygen)
References
- ↑ 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.
- ↑ 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.
- ↑ Zhao J, Cui Z, Yang R, Jia XY, Zhang Y, Zhao MH (2009). “Anti-glomerular basement membrane autoantibodies against different target antigens are associated with disease severity”. Kidney Int. 76 (10): 1108–15. doi:10.1038/ki.2009.348. PMID 19741587.
- ↑ Couser WG (2016). “Pathogenesis and treatment of glomerulonephritis-an update”. J Bras Nefrol. 38 (1): 107–22. doi:10.5935/0101-2800.20160016. PMID 27049372.
- ↑ Wilson CB, Dixon FJ (1973). “Anti-glomerular basement membrane antibody-induced glomerulonephritis”. Kidney Int. 3 (2): 74–89. PMID 4571918.
© 2026 MyEClinic – IFTM Institut für Telematik in der Medizin GmbH