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Schistosomiasis and the kidney.

Authors
  • Barsoum, Rashad S1
  • 1 Department of Internal Medicine, Cairo University, Cairo, Egypt. [email protected] , (Egypt)
Type
Published Article
Journal
Seminars in Nephrology
Publisher
Elsevier
Publication Date
Jan 01, 2003
Volume
23
Issue
1
Pages
34–41
Identifiers
PMID: 12563599
Source
Medline
License
Unknown

Abstract

Schistosomiasis is a parasitic infection that affects 200 million people and is directly responsible for an annual death of 20,000 patients. Three species are responsible for most of the morbidity in humans: Schistosoma hematobium in Africa, S. mansoni in Africa and South America, and S. Japonicum in the Far East. Renal involvement occurs mostly with S. hematobium infection as a consequence of fibrosis and calcification of tissue-trapped ova in the lower urinary tract, leading to obstruction, reflux, infection, and stone formation. The resulting interstitial nephritis may present with tubular dysfunction syndrome before it progresses to end-stage renal disease. The bladder lesions also are precancerous. Immune complexes containing S. hematobium or S. mansoni worm antigens may deposit in the glomeruli leading to 5 classes of glomerulonephritis: mesangioproliferative; exudative; mesangiocapillary (membranoproliferative); focal segmental sclerosis; and amyloidosis. Exudative lesions occur in the presence of Salmonella coinfection. Membranoproliferative and focal segmental sclerosis correlate with the degree of associated schistosomal hepatic fibrosis, with immunoglobulin (Ig) A playing a major role in their pathogenesis. Amyloidosis occurs in prolonged infection and correlates with the antigen load. Although the acute and early chronic lesions regress under antiparasitic treatment (eg, praziquantel), chronic sequelae are irreversible. End-stage renal disease obviously requires dialysis and transplantation.

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