Infectious glomerulopathy induced by a defined agent (Schistosoma mansoni): progression despite early elimination of the causal agent.

Abstract

Thirty Syrian golden hamsters were infected with Schistosoma mansoni and 10 were used as negative controls. Hamsters were infected by 50 cercaria; 15 were treated by praziquantil in doses of 100 mg/kg at 12, 13, 14 and 15 weeks postinfection, and 15 hamsters were left as positive control. Five from each subgroup were sacrificed at 24, 28 and 32 weeks postinfection. Animals were subjected to weekly analysis for total plasma protein, serum creatinine, albumin, cholesterol, 24-hour urine volume, and urinary total protein excretion. At the end point, animals were sacrificed and the mesenteric venous plexus was explored for adult worms. Kidney and liver specimens were examined by light microscopy, immunofluorescence microscopy, and electron microscopy. Complete parasite eradication was achieved in treated animals. Although there were significantly higher plasma total protein, albumin, and lower cholesterol in the treated group, there were no significant differences in proteinuria or renal histopathologic changes between treated and untreated animals. We conclude that in golden hamsters, with complete and early parasite eradication no regression occurs in S. mansoni-related nephropathy. Moreover, we suggest that in this glomerulopathy, short exposure to an antigen may be sufficient to set in motion a cascade of events which is irreversible and which leads to permanent glomerular damage.