Changing concepts in pathogenesis and morphology of analgesic nephropathy as seen in Europe

A causal connection between prolonged ingestion of phenacetin-containing analgesics and renal damage seems to be well established. Our concepts of the morphology and pathogenesis of analgesic nephropathy (AN), however, have changed since the first description by Spühler and Zollinger [1]. It was formerly believed that the initial lesion was chronic interstitial nephritis in the renal cortex with secondary papillary necrosis. With greater experience of the disease, it became apparent that papillary necrosis was the primary and predominant lesion and that the cortical changes were secondary to it. The historical aspects have been treated in detail by Gsell [2] and Heptinstall [3]