Pathophysiology of drug-induced papillary necrosis.
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.
D000143:Acids / Q000652:urine; D000208:Acute Disease; D058186:Acute Kidney Injury / Q000503:physiopathology; D000818:Animals; D002908:Chronic Disease; D004195:Disease Models, Animal; D004285:Dogs; D004573:Electrolytes / Q000652:urine; D005021:Ethylamines / Q000633:toxicity; D006801:Humans; D007671:Kidney Concentrating Ability; D007676:Kidney Failure, Chronic / Q000503:physiopathology; D007678:Kidney Glomerulus / Q000098:blood supply; D007679:Kidney Medulla / Q000502:physiology; D007681:Kidney Papillary Necrosis / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D011817:Rabbits; D051381:Rats; D012079:Renal Circulation / Q000187:drug effects
D000143:Acids; D004573:Electrolytes; D005021:Ethylamines; C004504:2-bromoethylamine