Acute urinary retention was produced in 15 adult mongrel dogs by ligation of the ureters. Studies of the hemostatic mechanism were made as the uremia progressed. All animals developed a coagulation defect characterized by abnormally long clotting time of whole blood in siliconized glassware. Other indices of coagulation efficiency were found to be normal or only slightly impaired.

It is not clear whether the basic defect is a lack of an essential clotting factor or an excess of an inhibitor. Urea does not seem to be the cause of the defect. The data suggest that the duration of urinary retention is as important as the degree of azotemia.

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