Experimental canine renal failure was studied as a potential animal model for human uremic bleeding. Renal failure accompanied by hemostatic alterations was induced in eight dogs by means of two surgical techniques of renal mass reduction. The hemostatic deficits consisted of immediate and marked reduction of the platelet glass bead retention (PR) to less than 10% of normal and gradual prolongation of the buccal mucosal bleeding time (BMBT) to approximately four times the normal value. Platelet count, volume, aggregation responses, and coagulation were normal. A packed cell volume (PCV) of less than 30% was observed in three dogs. Elevation of the PCV normalized the BMBT in two dogs, but because the PR was unchanged and the BMBT effect was temporary, anemia was not considered the primary cause of the prolonged bleeding time. There was a significant, positive correlation between BMBT and BUN, suggesting that the altered hemostasis may be related to the accumulation of urea or other uremic toxins of protein origin. The finding of a defect in PR and BMBT--tests that require normal platelet adhesion and aggregation--in azotemic dogs were platelet numbers and aggregation are normal indirectly implicates platelet adhesion as the primary hemostatic defect.