The case was a 54-year-old woman who had suffered from occasional incontinence of urine after a craniotomy for subarachnoid hemorrhage in 1991. In June 1998 she was admitted for nephrotic syndrome without hematuria. Intravenous pyelography and voiding cystourethrography revealed bilateral hydronephrosis, atonic bladder, and vesicoureteral reflux (VUR). Renal biopsy demonstrated the presence of focal segmental glomerulosclerosis with cellular lesions. However, periodic-acid methenamine silver (PAM) staining revealed bubbling and spike appearance in the diffuse peripheral loops, although immunofluorescence microscopy showed negative findings in the glomeruli. Electron microscopy revealed diffuse thickening of the glomerular basement membrane (GBM) accompanying diffuse podocytic infolding lesions into the GBM and numerous spherical microstructures in the GBM. No findings of dense deposits were observed in the GBM and mesangium. Her urinary protein excretion decreased and renal function improved after placement of an urethral catheter for one year. A second renal biopsy revealed a remarkable decrease in podocytic infolding lesions, although microstructures in the GBM remained. Although mechanisms of the occurrence of these peculiar podocytic infolding lesions are unclear, it is speculated that podocyte damage due to hydronephrosis may have caused the lesions.

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