Lack of Role of Platelet Aggregation on 2-Bromoethylamine Hydrobromide-induced Renal Papillary Necrosis in Rats

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We investigated the role of platelet aggregation on 2-bromoethylamine hydrobromide-induced renal papillary necrosis by using the rats treated with antiplatelet drug. Ten male Sprague-Dawley rats were orally administered with ticlopidine hydrochloride at 300 mg/kg/day for 5 successive days. Ten control rats were orally administered with the vehicle. Five rats in each group were injected intraperitoneally with 2-bromoethylamine hydrobromide at 100 mg/kg at 1 hr after the 3rd administration of ticlopidine or the vehicle and the remaining five rats in each group received saline in the same manner. On the last day of the treatment, blood was collected and ADP-induced platelet aggregation was measured. The kidneys were examined microscopically and the area of total renal papillary necrosis was measured. Platelet aggregation was significantly inhibited in ticlopidine-treated rats. However, renal papillary necrosis was observed in all rats injected with 2-bromoethylamine hydrobromide and there was no difference in the area of renal papillary necrosis between ticlopidine and vehicle-treated groups. These data showed that platelet aggregation did not contribute to the development of 2-bromoethylamine hydrobromide-induced renal papillary necrosis in rats.