Abstract
Renal papillary necrosis (RPN) has been associated with the long-term abuse of mixed analgesics and therapeutic doses of non-steroidal anti-inflammatory drugs (NSAIDs). Chronic renal failure and upper urothelial carcinoma are frequently associated with analgesic abuse, but their relationship to RPN is less certain (Bach and Bridges 1985). Attempts to define the molecular basis of RPN using analgesics have not been successful in experimental animals because of extrarenal toxicity and a highly variable RPN. Also there are no clinical biochemistry tests that identify these changes until they progress towards renal failure, and focal necrosis is easily missed by routine histopathology unless sections go through the papilla tip (Bach and Bridges 1985; Bach and Hardy 1985).
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