Experimental papillary necrosis of the kidney. I. Morphologic and functional data.
Papillary necrosis was produced in rats by a single intravenous injection of bromoethylamine hydrobromide (BEA). The earliest changes as seen by light microscopy were necroses of the limbs of Henle and eosinophilic droplets in collecting ducts. Complete necrosis of the papilla took place between 4 and 7 days and the dead papilla was usually sequestered completely by 21 days. Cortical changes occurred secondary to papillary necrosis. Tubular atrophy and loss was greatest in the deeper parts of the central cortex, the more superficial nephrons frequently being spared. The perihilar cortex was the least involved. This distribution was considered to be related to the respective lengths of the limbs of Henle, nephrons with limbs extending into the papilla being those undergoing change. Increased urine output occurred during the first day and continued thereafter. There was a profound defect in concentrating ability.
D000818:Animals; D001806:Blood Urea Nitrogen; D001966:Bromine; D004195:Disease Models, Animal; D005021:Ethylamines; D005260:Female; D007668:Kidney / Q000473:pathology; D007671:Kidney Concentrating Ability; D007681:Kidney Papillary Necrosis / Q000139:chemically induced / Q000473:pathology* / Q000503:physiopathology; D009994:Osmolar Concentration; D051381:Rats; D014556:Urine
D005021:Ethylamines; D001966:Bromine