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THERE IS A GROWING BODY of clinical evi-dence suggesting a relationship be-tween the excessive ingestion of analgesic medication and the development of chronic renal disease. The evidence is almost wholly circumstantial in character, and the avail-able epidemiologic data are suggestive but not thoroughly convincing (1, 2). Aceto-phenetidin (phenacetin) or some metabolic product thereof has been the suspected of-fending agent in analgesic preparations on similar grounds. Although many efforts have been made to develop a reproducible experimental renal disease in laboratory animals using the ingredients of analgesic preparations, most have met with failure,
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Christopher C. Fordham (1965) studied this question.
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