Renal and urinary lipid changes associated with an acutely induced renal papillary necrosis in rats

A single dose of 2-bromoethanamine hydrobromide (BEA; 100 mg/kg body weight) given ip to male Wistar rats causes an acute renal papillary necrosis in 24 hr. Oil Red O (ORO) lipid staining is normally confined to the polyunsaturated lipid droplets of the medullary interstitial cells, but ORO-positive material was present in the endothelial cells of the vasa recta 7 hr after BEA treatment. At 24 hr (by which time papillary necrosis had developed), there were also markedly increased quantities of lipid in the cells of the collecting ducts and covering epithelia. At 48 hr totally necrosed areas stained heavily with ORO, and lipid deposits were particularly numerous in the hyperplastic urothelia adjacent to the necrosed region. Epithelial and endothelial accumulation of lipid material also extended into areas of the juxtamedulla and cortex, which appeared normal by routine haematoxylin and eosin staining. Lipid staining is more selective and sensitive for identifying papillary necrosis than routine histology, because neither hexachlorobutadiene-, aminoglycoside-, cis-platin- nor polybrene-induced lesions produce similar histochemical changes. This suggests that the capillary and epithelial deposits of lipid material are pathognomonic for the development of renal papillary necrosis. An increase in urinary triglycerides following BEA treatment supports the biochemical basis of these ORO changes as a neutral lipid accumulation.