Thromb Haemost 1987; 57(03): 263-268
DOI: 10.1055/s-0038-1651113
Original Article
Schattauer GmbH Stuttgart

Antithrombin III and Heparin Cofactor II in Patients with Chronic Renal Failure Undergoing Regular Hemodialysis

P Toulon
1   The Laboratoire d’hématologie, UER de Biologie expérimentale et humaine, Paris, France
,
C Jacquot
2   The AURA, Paris, France
,
L Capron
3   The Centre de recherche Claude-Bernard en Pathologie vasculaire (Pr Housset), Hôpital Broussais, Paris, France
,
M -O Frydman
2   The AURA, Paris, France
,
D Vignon
4   The Poste de transfusion, Hôpital Foch, Suresnes, France
,
M Aiach
1   The Laboratoire d’hématologie, UER de Biologie expérimentale et humaine, Paris, France
› Author Affiliations
Further Information

Publication History

Received 05 December 1986

Accepted after revision 10 February 1987

Publication Date:
06 July 2018 (online)

Summary

Heparin enhances the inhibition rate of thrombin by both antithrombin III (AT III) and heparin cofactor II (HC II). We studied the activity of these two plasma proteins in patients with chronic renal failure (CRF) undergoing regular hemodialysis as their heparin requirements varied widely. In 77 normal blood donors, normal ranges (mean ± 2 SD) were 82-122% for AT III and 65-145% for HC II. When compared with these controls 82 dialyzed CRF patients had a subnormal AT III activity and a significantly (p <0.001) lower HC II activity. To evaluate the effect of hemodialysis we compared AT III, HC II and total proteins in plasma before and after dialysis in. 24 patients (12 with normal and 12 with low basal HC II activity). AT III and HC II activities significantly (p <0.001) increased in absolute value. When related to total plasma proteins, in order to suppress the influence of hemoconcentration induced by dialysis, AT III decreased significantly (p <0.01) whereas HC II increased slightly but significantly (p <0.01) in the 12 patients with low initial HC II activity. The decrease of AT III induced by heparin administrated during dialysis is likely to account for this relative decrease of AT III activity. A modification of the distribution of both HC II and heparin between the vascular wall and the circulating blood is evoked to explain the relative increase in HC II activity and the need for higher heparin dosage in patients with low HC II levels.

 
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