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One hundred and twenty Syrian golden hamsters were infected with Schistosoma mansoni cercariae and 20 served as negative controls (group I). Of the S. mansoni-infected hamsters, 20 served as positive controls (group II) and 100 hamsters were treated for 12 weeks post-infection by loading with S. mansoni adult worm antigen. Animals were divided into groups according to the dose of adult worm antigen injected: group III (5-fold increase in circulating antigen concentration), group IV (10-fold increase), group V (20-fold increase), group VI (40-fold increase), and group VII (80-fold increase). Each of the groups was subdivided into four groups (sacrificed at 1, 2, 4 or 7 days after initiation of antigen loading or the corresponding time points in the case of the control groups). At sacrifice, blood and urine were obtained for laboratory assessment (serum creatinine, protein, albumin, cholesterol and urinary proteins). Kidney, liver and spleen tissue specimens were obtained for light, immunofluorescent and electron microscopic examinations. At sacrifice, significant proteinuria, hypoalbuminaemia and hypercholesterolaemia were observed in S. mansoni-infected hamsters when compared with negative control animals. Histopathologic assessment showed changes compatible with those previously reported, mainly immune complex glomerular deposits, mesangial proliferation and renal amyloid deposits. Significant laboratory improvement was observed in animals treated with antigen loading, especially those treated with 80-fold antigen excess and sacrificed at 7 days postinitiation of treatment. Histopathologic evaluation showed significantly less immune complex glomerular deposits, less mesangial hyperplasia, and less amyloid deposits in hamsters treated with antigen loading. It is concluded that induction of antigen excess by antigen loading induces biochemical and histopathologic regression of schistosomal-specific nephropathy in S. mansoni-infected Syrian golden hamsters.

Schistosomal-specific nephropathy in Syrian golden hamsters: treatment by induction of antigen excess