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Nephrol Dial Transplant (2002) 17: 4-7
© 2002 European Renal Association-European Dialysis and Transplant Association


Editorial Comments

Human Schistosoma mansoni-associated glomerulopathy in Brazil

Israel Nussenzveig1,, Thales De Brito2, Celia Regina W. Carneiro3 and Ana Maria G. Silva2

1 Division of Nephrology, ‘Hospital das Clinicas’, 2 Institute of Tropical Medicine, University of São Paulo Medical School and 3 Department of Microbiology, Immunology and Parasitology, Federal University of São Paulo, Medical School, São Paulo, SP, Brazil

Keywords: differential diagnosis; geographical differences; pathology

Introduction

A recent immuno-electron microscopy (IM-EM) study was conducted on a series of patients with [1] schistosomal glomerulopathy (SG) using a monoclonal anti-Schistosoma mansoni antibody obtained from adult worms. IM-EM allows precise localization of schistosomal antigen deposits in glomerular structures. Based on this work and on the experience accumulated along the years with this disease at the Institute of Tropical Medicine and at the Nephrology Division of the ‘Hospital das Clinicas’ (São Paulo University Medical School), we review here the difficulties involved in diagnosing SG and emphasize some differences from the Egyptian equivalent reviewed by Barsoum et al. [2,3].

In his editorial review, Barsoum [2] suggested the classification of SG into five histopathological categories: mesangio-proliferative glomerulonephritis (GN), membrano-proliferative glomerulonephritis, focal and segmental glomerulosclerosis (FSGS), exudative glomerulonephritis and amyloidosis. Exudative glomerulonephritis was associated with chronic salmonellosis, amyloidosis and with both recurrent salmonellosis and . . . [Full Text of this Article]

Mesangio-proliferative and membrano-proliferative glomerulonephritis

Schistosomal glomerulopathy and hepato-intestinal mansonian schistosomiasis

Differential diagnosis

Schistosomal glomerulopathy and FSGS

Schistosomal glomerulopathy, membranous nephropathy and minimal-change disease

Alternative hypothesis

Amyloidosis

Schistosomal glomerulopathy and IgA deposits

Conclusions

Acknowledgments

Notes

References


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