Pathology, aetiology and pathogenesis of analgesic nephropathy.
1. The initial site of damage in analgesic abuse is the renal medulla and the characteristic lesion is renal papillary necrosis. The papillary necrosis appears to be an ischaemic infarct. The cortical lesion of chronic interstial nephritis is a non-specific change and secondary to obstruction to tubules in the necrotic medulla. 2. Medullary perfusion and the concentration mechanism appear to be important factors in the genesis of renal papillary necrosis. 3. Experimental and clinical studies suggest that abuse of compound analgesics containing aspirin, phenacetin and caffeine result in renal papillary necrosis and the clinical syndrome of analgesic nephropathy. In the APC mixture aspirin appears to be the major nephrotoxic agent while phenacetin plays a synergistic but secondary role in the renal nephrotoxicity.
D000818:Animals; D001172:Arthritis, Rheumatoid / Q000150:complications; D001241:Aspirin / Q000009:adverse effects* / Q000633:toxicity; D004338:Drug Combinations; D006801:Humans; D007672:Kidney Cortex / Q000473:pathology; D007679:Kidney Medulla / Q000473:pathology; D007681:Kidney Papillary Necrosis / Q000139:chemically induced* / Q000150:complications / Q000473:pathology; D010615:Phenacetin / Q000009:adverse effects* / Q000633:toxicity; D051381:Rats
D004338:Drug Combinations; D010615:Phenacetin; D001241:Aspirin