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Schistosomiasis and glomerular disease

Rashad S Barsoum, MD, FRCP, FRCPE
Section Editors
Richard J Glassock, MD, MACP
Brad H Rovin, MD
Deputy Editor
Albert Q Lam, MD


Human schistosomiasis is caused by infection with Schistosoma haematobium, S. mansoni, S. japonicum, S. mekongi, or S. intercalatum. The glomerular disease associated with schistosomiasis will be discussed here. Other issues related to schistosomiasis are presented separately. (See "Epidemiology, pathogenesis, and clinical manifestations of schistosomiasis" and "Diagnosis of schistosomiasis" and "Treatment and prevention of schistosomiasis".)


Like many other helminthic diseases [1], schistosomiasis may produce a broad spectrum of glomerular pathology. The incidence is unknown since many cases are subclinical or resolve spontaneously. In a village in Upper Egypt, for example, where S. haematobium was newly introduced as a result of changing irrigation methods, the majority of those who acquired the infection developed self-limited nephrotic-range proteinuria with biopsy-confirmed mesangioproliferative glomerulonephritis [2,3]. Similar glomerular lesions have also been described with recent S. mansoni or S. japonicum infection and usually resolve with antiparasitic treatment.

In contrast, persistent or progressive glomerular disease develops in approximately 10 to 15 percent of patients who usually have hepatic fibrosis due to chronic infection with S. mansoni (and occasionally S. haematobium) [4-8].


Several observations are compatible with a pathogenic role for the immune response to the parasite in the development of glomerulonephritis in affected patients:

Glomerular lesions, similar to those described in humans, have been induced by experimental infection of many small and large animals [9].


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Literature review current through: Sep 2016. | This topic last updated: Jul 6, 2015.
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