Enzyme histochemical changes in an acutely induced renal papillary necrosis.

Enzyme histochemistry was assessed in semi-thin glycolmethacrylate sections after 100 mg/kg 2-bromoethanamine (BEA) hydrobromide had been given ip to male Wistar rats to induce renal papillary necrosis. Changes in the proximal tubular marker enzymes alkaline phosphatase (Alk Phos), gamma-glutamytranspeptidase (GGT) and adenosine triphosphatase (ATPase) were not apparent before 8 hr, but there was a progressive loss up to 144 hr. The proteinaceous PAS-positive casts in the loops of Henle and the collecting ducts stained for Alk Phos and GGT (from 12 hr) and for ATPase (from 18 hr). Acid phosphatase (Acid Phos) staining was increased in the proximal tubule lysosomes from 18 hr. There was a marked increase in Alk Phos in all hyperplastic upper urothelial cells from 8 to 24 hr, and a mosaic of staining remained in the pelvis adjacent to the necrosed papilla at 144 hr. At 12 hr, there was an increase in the staining of the pelvic, ureter and bladder vascular endothelial ATPase, the intensity and area of which increased progressively from 18 hr and almost occluded the capillary lumens in the worst affected areas by 144 hr. These data show several distinct series of pathological changes after the administration of BEA. The subtle degenerative changes in the proximal tubule followed the papillary lesion, but exfoliated brush border and proximal tubular cells were important components of the protein casts in the distal nephron. Similarly, the intense Alk Phos staining in the hyperplastic regions of the upper urothelium and the increased pelvic, ureteric and bladder endothelial ATPase staining suggested they develop as a consequence of the papillary lesion.