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© 1984 Oxford University Press

research-article

Pathophysiology of Drug-Induced Papillary Necrosis1

SANDRA SABATINI

Section of Nephrology, University of Illinois College of Medicine Chicago, Illinois 60612

Pathophysiology of Drug-Induced Papillary Necrosis. SABATINI, S. (1984). Fundam, Appl. Toxicol. 4, 909–921. Papillary necrosis, a common cause of renal failure, is a life-threatening pathophysiologic event which may have a multiplicity of mechanisms. The primary functional lesions are salt wastage, impairment of urinary concentrating ability, polyuria, and imbalances of potassium, calcium and phosphate homeostasis; urinary acidification is completely normal. Papillary necrosis is associated with a profound decrease in juxtamedullary nephron glomerular filtration rate, in addition to damage to the papillary collecting duct. 2-Bromoethylamine hydrobromide (BEA) has proved to be a useful tool in elucidating the generation of this important clinical syndrome


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