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Histopathology of chronic renal allograft dysfunction

Transplantation Reviews, ISSN: 0955-470X, Vol: 18, Issue: 2, Page: 80-85
2004
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Article Description

The rate of late allograft loss remains relatively constant, despite greatly improved success in the early management of renal transplants. The pathological changes encountered in kidneys undergoing late allograft dysfunction are the result of a variety of processes, both immune and nonimmune. The gradual appearance of interstitial fibrosis and tubular atrophy is a nonspecific finding, which characterizes late allograft dysfunction. Features that indicate chronic rejection include transplant glomerulopathy, vascular intimal hyperplasia, particularly in association with intimal lymphocytic infiltration. Both of these changes may be related to humoral rejection. Animal models provide important insights into the mechanism of chronic rejection. In a commonly used model, the Fisher to Lewis rat model, antidonor antibodies against matrix proteins are associated with the development of transplant glomerulopathy, and the appearance of antitubular antibodies and a granulomatous interstitial nephritis may indicate graft-host differences in tubular basement membrane structure.

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