Focal segmental glomerulosclerosis in a 32-year-old kidney allograft after 7 years without immunosuppression.

In kidney allografts, focal segmental glomerulosclerosis (FSGS) has been described as recurrent, de novo, or a histological variant of chronic transplant glomerulopathy. We describe a unique case of de novo FSGS in a renal transplant not accompanied by any feature of rejection in a patient who had not been immunosuppressed for several years. A 58-year-old woman received a histoidentical living-related kidney transplant for end-stage renal disease due to chronic pyelonephritis. Twenty-four years after the transplant she voluntarily discontinued all immunosuppressive medication. Seven years later she presented with nephrotic syndrome, mild renal failure, and positive serology for hepatitis C virus (HCV) antibody. The kidney transplant biopsy disclosed de novo FSGS. Features of acute or chronic rejection, including chronic transplant glomerulopathy, were not seen. The pathogenesis of this lesion is probably related to sustained and prolonged glomerular hyperfiltration; alternatively, HCV infection may have triggered or accelerated the appearance of FSGS.

Citrate transport in rabbit nephron.

Citrate is an important renal metabolic substrate and urinary inhibitor of calcium stone formation. Our purpose was to characterize citrate reabsorption in the rabbit nephron using isolated perfused tubules. Citrate reabsorption, measured by luminal disappearance of [14C]citrate, was found only in the proximal tubule, not in the cortical thick ascending limb or the cortical collecting tubule. In the proximal convoluted tubule, the collected fluid was also analyzed by thin-layer chromatography and by measurements of chemical citrate concentration using an ultramicroassay. Luminal disappearance of [14C]citrate was determined to accurately represent citrate reabsorption; no significant citrate secretion was found. The absolute magnitude of citrate reabsorption was approximately 3.4 pmol X mm-1 X min-1 using either 1 or 3 mM citrate in the perfusate. This rate of citrate reabsorption in the rabbit proximal tubule could account for all of renal citrate reabsorption but was severalfold lower than glucose reabsorption, which was studied for comparative purposes. In contrast, the magnitude of succinate transport (which probably occurs via the same transport system as citrate) was comparable with that of citrate. Citrate reabsorption was inhibited approximately 80% by 10(-5) M ouabain. This characterization of citrate transport in the intact proximal tubule should provide a useful model to study regulation of urinary citrate excretion.