The pertinent literature concerning the experimental induction of analgesic nephropathy is reviewed. Based on the accumulated data from animal experiments that induced a pathologic lesion resembling chronic analgesic nephropathy, of the limited number of analgesics tested, aspirin seems to be the most nephrotoxic of the commonly available analgesics. When aspirin is combined with other analgesics, the limited data available suggest at least an additive nephrotoxic effect, if not a synergism. The histologic presentation of acute intoxication is substantially different from that following chronic ingestion. With improvements in pathologic analysis of experimental results, future studies may well provide more insight as to the significance, relative contribution, and risk of combination analgesic products in inducing experimental analgesic nephrotoxicity.
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