Drug-induced papillary necrosis: electrolyte excretion and nephron heterogeneity.

The functional expression of papillary necrosis was investigated in rats following administration of 2-bromoethylamine hydrobromide (BEA). The percentage of filtering superficial and juxtamedullary nephrons was assessed using the qualitative Hanssen technique. There was a marked decrease in the percentage of filtering juxtamedullary nephrons 24 h after the induction of papillary necrosis (as compared with control rats), which was blunted in salt-loaded animals. The percentage of filtering superficial nephrons was the same in all three groups. BEA administration to normal rats was associated with a significant increase in sodium, chloride, phosphate, and calcium excretion. BEA administration to rats on a chloride-restricted diet was associated with chloride wastage. These animals also failed to adapt to a low chloride diet as late as 7 days after the administration of BEA. The phosphaturia observed in intact rats treated with BEA was abolished by parathyroidectomy. BEA-treated rats were able to adapt to a low phosphate diet and to a low magnesium diet. These data demonstrate that papillary necrosis is associated with profound impairment of juxtamedullary nephron filtration and with chloride wastage. In the absence of the papillary structures adaptation to phosphorus or magnesium deprivation is still possible.