Experimental Analgesic Nephropathy

The renal and other organ damage induced by mild analgesics in animals under acute or subacute conditions is not specific to analgesics; it may have a relationship to acute poisoning in man but is not related to human nephropathy attributed to analgesic abuse. Chronic experiments with single or mixed analgesics conducted under stringent scientific conditions are negative if the dose levels are not lethal. Dehydration combined with high dose levels of analgesics produces papillary necrosis in rats but such experiments are not relevant to human analgesic nephropathy. The dependence of phenacetiri metabolism on the dose level administered, demonstrated by the increased formation of potentially toxic metabolites, has great importance for the understanding of analgesic nephropathy in man. This type of nephropathy seems to be specific for humans; the immunologic theory affirming the role of the antigen of p-phenetidine is the most plausible but needs further confirmation. Results in the field of analgesic-induced experimental kidney damage indicate that had pathologists and clinicians not drawn attention to the problem of nephropathy caused by analgesic abuse, the toxicologists would never have suspected, forseen, or predicted the appearence of such a syndrome.