Goodpasture syndrome epidemiology and demographics

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] Akshun Kalia M.B.B.S.[4]

Overview

The prevalence of Goodpasture syndrome worldwide is an estimated 1 case per million individuals, with high prevalence in Caucasians. The peak incidence of the disease occurs between the ages of 20 and 30 and again at 60 and 70. Goodpasture syndrome affects men and women equally.

Epidemiology and Demographics

Incidence

The incidence of Goodpasture syndrome is approximately 0.18 cases per 100,000 individuals worldwide.^[1]
The annual incidence of Goodpasture syndrome in Europe is estimated to range from 0.5 to 1 per 1 million individuals .^[2]
The incidence of Goodpasture syndrome is around 1- 2 per million individuals per year.

Prevalence

The prevalence of Goodpasture syndrome is estimated to be 1 per million individuals annually.^[3]

Age

Goodpasture syndrome occurs in two age peaks.^[4]
The early onset Goodpasture syndrome is seen with individuals in the age group of 20 and 30.
The late onset Goodpasture syndrome is seen with individuals in the age group of 60 to 70.

Gender

Goodpasture syndrome affects men and women equally.^[4]
Males are at increased risk of developing Goodpasture syndrome in the second and third decade.
Females are at an increased risk of developing the syndrome in the sixth to seventh decade.

Race

Goodpasture syndrome usually affects individuals of the white race. Black individuals are less likely to develop Goodpasture syndrome.
In European populations between 0.5-1 case per million individuals are seen every year. It is rarer in non-European populations.

Region

The majority of Goodpasture syndrome cases are reported in ethnic groups of New Zealand.

References

↑ Kluth DC, Rees AJ (1999). “Anti-glomerular basement membrane disease”. J Am Soc Nephrol. 10 (11): 2446–53. PMID 10541306.
↑ Fomegné G, Dratwa M, Wens R, Mesquita M, Van der Straaten M, Vanden Haute K; et al. (2006). “[Goodpasture disease]”. Rev Med Brux. 27 (3): 162–6. PMID 16894954.
↑ Tang W, McDonald SP, Hawley CM, Badve SV, Boudville NC, Brown FG, Clayton PA, Campbell SB, de Zoysa JR, Johnson DW (March 2013). “Anti-glomerular basement membrane antibody disease is an uncommon cause of end-stage renal disease”. Kidney Int. 83 (3): 503–10. doi:10.1038/ki.2012.375. PMID 23254902.
↑ ^4.0 ^4.1 Cui Z, Zhao MH (2011). “Advances in human antiglomerular basement membrane disease”. Nat Rev Nephrol. 7 (12): 697–705. doi:10.1038/nrneph.2011.89. PMID 21769105.

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[pmid10541306-1] Kluth DC, Rees AJ (1999). “Anti-glomerular basement membrane disease”. J Am Soc Nephrol. 10 (11): 2446–53. PMID 10541306.

[pmid16894954-2] Fomegné G, Dratwa M, Wens R, Mesquita M, Van der Straaten M, Vanden Haute K; et al. (2006). “[Goodpasture disease]”. Rev Med Brux. 27 (3): 162–6. PMID 16894954.

[pmid23254902-3] Tang W, McDonald SP, Hawley CM, Badve SV, Boudville NC, Brown FG, Clayton PA, Campbell SB, de Zoysa JR, Johnson DW (March 2013). “Anti-glomerular basement membrane antibody disease is an uncommon cause of end-stage renal disease”. Kidney Int. 83 (3): 503–10. doi:10.1038/ki.2012.375. PMID 23254902.

[pmid21769105-4] 4.0 ^4.1 Cui Z, Zhao MH (2011). “Advances in human antiglomerular basement membrane disease”. Nat Rev Nephrol. 7 (12): 697–705. doi:10.1038/nrneph.2011.89. PMID 21769105.

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