INFECTIOUS GLOMERULOPATHY INDUCED BY A DEFINED AGENT (SCHISTOSOMA-MANSONI) - PROGRESSION DESPITE EARLY ELIMINATION OF THE CAUSAL AGENT

Thirty Syrian golden hamsters were infected with Schistosoma mansoni a nd 10 were used as negative controls. Hamsters were infected by 50 cer caria; 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 wee ks 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 adu lt worms. Kidney and liver specimens were examined by light microscopy , immunofluorescence microscopy, and electron microscopy. Complete par asite eradication was achieved in treated animals. Although there were significantly higher plasma total protein, albumin, and lower cholest erol in the treated group, there were no significant differences in pr oteinuria or renal histopathologic changes between treated and untreat ed animals. We conclude that in golden hamsters, with complete and ear ly parasite eradication no regression occurs in S. mansoni-related nep hropathy. Moreover, we suggest that in this glomerulopathy, short expo sure to an antigen may be sufficient to set in motion a cascade of eve nts which is irreversible and which leads to permanent glomerular dama ge.