Chemically induced renal papillary necrosis and upper urothelial carcinoma. Part 2

• Published in: CRC critical reviews in toxicology Vol. 15; no. 4; p. 331
• Main Authors: Bach, P H, Bridges, J W
• Format: Journal Article
• Language: English
• Published: United States 1985
• Subjects: Analgesics - toxicity; Animals; Anti-Inflammatory Agents - toxicity; Arachidonic Acid; Arachidonic Acids - metabolism; Biotransformation; Carcinogens - metabolism; Dogs; Glycoproteins - metabolism; Guinea Pigs; Humans; Hyperbilirubinemia - complications; Hyperplasia; Ischemia - complications; Kidney - pathology; Kidney - physiopathology; Kidney Medulla - blood supply; Kidney Medulla - metabolism; Kidney Papillary Necrosis - chemically induced; Kidney Papillary Necrosis - pathology; Kidney Papillary Necrosis - physiopathology; Lipids - biosynthesis; Mice; Microcirculation - pathology; Peroxidases - physiology; Phenacetin - metabolism; Phenacetin - toxicity; Prostaglandins - metabolism; Rats; Species Specificity; Urinary Bladder - pathology; Urinary Bladder Neoplasms - chemically induced; Urinary Bladder Neoplasms - pathology; Urinary Bladder Neoplasms - physiopathology
• ISSN: 0045-6446
• DOI: 10.3109/10408448509056267

In the past, renal papillary necrosis (RPN) has been commonly associated with long-term abusive analgesic intake, but over recent years a wide variety of industrially and therapeutically used chemicals have been shown to induce this lesion experimentally or in man. Destruction of the renal papilla may result in: (1) secondary degenerative cortical changes which precede chronic renal failure or (2) a rapidly metastasizing upper urothelial carcinoma, which has a very poor prognosis. This article will briefly review the published data on the morphology, function, and biochemistry of the normal renal medulla and the pathology associated with RPN, together with the secondary changes which give rise to cortical degeneration or epithelial carcinoma. It will then examine in detail those chemicals which have been reported to cause RPN in an attempt to delineate structure-activity relationships. Finally, the many different theories that have been proposed to explain the pathophysiology of RPN will be examined and an hypothesis will be put forward to explain the primary pathogenesis of the lesion and its secondary consequences.