Experimental renal disease due to schistosomiasis.
Although there is a marked variability in the development of renal lesions among individual animal models of schistosomal infections, much has been learned about the mechanisms leading to renal injury. The lesions in S. mansoni and S. japonicum infections correspond quite closely to the immune complex type of lesions, with complement involvement. The main antigens involved seem to be polysacharides of worm-gut origin, but participation of other antigens (including soluble egg antigens) cannot be excluded. Many observations testify to the localization of immune complexes, preformed in circulation, but the possibility that antigens, filtered through glomeruli, deposit incapillary walls first and bind with corresponding antibodies later on should be considered also. Deoxyribonucleic acids also may play a role in the pathogenesis. The perpetuation of the lesions is probably due to constant supply of antigens. In some models, renal pathology was related to the dose of infection, but in others there was no relation to worm burden. Renal pathology in S. haematobium infections is different, being related to the lower urinary tract, with obstructive lesions causing pyelonephritis and hydronephrosis.
D000818:Animals; D000936:Antigen-Antibody Complex; D006224:Cricetinae; D004195:Disease Models, Animal; D005260:Female; D000882:Haplorhini; D006801:Humans; D007075:Immunoglobulin M; D007674:Kidney Diseases / Q000209:etiology* / Q000469:parasitology* / Q000473:pathology; D007678:Kidney Glomerulus / Q000473:pathology; D008251:Macaca; D008253:Macaca mulatta; D051379:Mice; D002679:Pan troglodytes; D010215:Papio; D011817:Rabbits; D012549:Schistosoma japonicum / Q000276:immunology; D012550:Schistosoma mansoni / Q000276:immunology; D012552:Schistosomiasis / Q000276:immunology*
D000936:Antigen-Antibody Complex; D007075:Immunoglobulin M