Pathology of analgesic nephropathy: Australian experience.
Analgesic nephropathy was first studied in Switzerland and Scandinavia, and most observers thought that papillary necrosis, a feature of the pathology, was the result of chronic interstitial nephritis, the other principal feature. From 1962, reports indicated a high incidence of analgesic nephropathy in Australia and suggested that papillary changes preceded cortical damage. Later, associated uroepithelial carcinoma was noted. Early papillary lesions consist of necrosis of elements around groups of collecting ducts. Necrosis extends upward through the medulla from the papilla and gradually intensifies to total papillary destruction. Fat and calcium accumulation and changes in matrix mucopolysaccharide are markers of papillary injury. Cortical atrophy is dependent upon collecting duct obstruction and is proportional to the degree of obstruction. Infection may complicate late pathologic changes. It is suggested that in the early stages the disease represents an injury to "concentrating columns" in the medulla.
D000700:Analgesics / Q000633:toxicity*; D001315:Australia; D006801:Humans; D007672:Kidney Cortex / Q000187:drug effects / Q000473:pathology; D007674:Kidney Diseases / Q000139:chemically induced* / Q000473:pathology; D007679:Kidney Medulla / Q000187:drug effects / Q000473:pathology; D007681:Kidney Papillary Necrosis / Q000139:chemically induced / Q000473:pathology; D007682:Kidney Pelvis / Q000187:drug effects / Q000473:pathology; D007685:Kidney Tubules, Collecting / Q000187:drug effects / Q000473:pathology; D009395:Nephritis, Interstitial / Q000139:chemically induced
D000700:Analgesics