Acute hyperuricemic nephropathy and renal failure after transplantation.
This report describes a patient who was treated for rejection of a cadaveric renal allograft with a variety of drugs, including the continuous administration of ciclosporin over a period of 16 months. The patient developed hyperuricemia, attacks of gout and finally a rapidly progressing renal failure 17 months after transplantation. The removed transplanted kidney showed extensive tubular dilatation, intratubular deposits of uric acid crystals and characteristic granulomas. There was also morphologic evidence of transplant glomerulopathy, as well as scattered linear parenchymal (cortical?) scars of the type seen in mild chronic ciclosporin toxicity. Both of these changes undoubtedly contributed to the reduction of renal reserve. However, we propose that prolonged continuous use of ciclosporin was the main factor in the development of hyperuricemia and obstructive hyperuricemic nephropathy and renal failure in this patient. To our knowledge cases of this nature have not been previously reported.
Venkataseshan
V S
VS
Department of Pathology, Mount Sinai School of Medicine, New York, N.Y.
Feingold
R
R
Dikman
S
S
Churg
J
J
D000328:Adult; D003524:Cyclosporins / Q000009:adverse effects / Q000627:therapeutic use; D006084:Graft Rejection; D006086:Graft vs Host Disease / Q000188:drug therapy; D006801:Humans; D007668:Kidney / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D007676:Kidney Failure, Chronic / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D016030:Kidney Transplantation / Q000009:adverse effects*; D008297:Male; D008854:Microscopy, Electron; D014527:Uric Acid / Q000097:blood* / Q000378:metabolism
D003524:Cyclosporins; D014527:Uric Acid