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K. N. von KAULLA, MD; E. von KAULLA, MD; S. WASANTAPRUCK, MD; T. L. MARCHIORO, MD; T. E. STARZL, MD

AMA Arch Surg. 1966;92(2):184-191.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

ALTHOUGH the bleeding tendency of patients with renal failure is well known, the literature concerning the cause of the coagulation failure is both meager and confusing. The hemostatic abnormality has been said to be greater in acute than in chronic uremia, and even to occur by a different mechanism.²¹ A variety of clotting defects have been described in both types of patients. Various plasma clotting factors have been found to be moderately reduced¹⁰ with inconstant hypofibrinogenemia,^8-10 with or without involvement of the prothrombin complex.^5,9 Abnormal thrombelastograms, reduced heparin tolerance,⁸ and prolonged thrombin time¹⁰ have also been seen in many, but not all, patients.

The most consistently reported coagulation abnormality of uremia has been a deficiency in prothrombin consumption.^{4,5,10, 21,22} In some cases, this could be explained solely by the thrombocytopenia which has been thought by some to be a common^9,21 and by . . . [Full Text PDF of this Article]

Author Affiliations
DENVER

From the departments of medicine and surgery, the University of Colorado School of Medicine and the Veterans Administration Hospital, Denver.

Footnotes
Submitted for publication Oct 19, 1965.

Reprint requests to 4200 E Ninth Ave, Denver, Colo 80220 (Dr. Starzl).

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