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Management of Heparin‐Induced Thrombocytopenia During Renal Replacement Therapy
Author(s) -
Davenport Andrew
Publication year - 2001
Publication title -
hemodialysis international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.658
H-Index - 47
eISSN - 1542-4758
pISSN - 1492-7535
DOI - 10.1111/hdi.2001.5.1.81
Subject(s) - medicine , hirudin , heparin , argatroban , bivalirudin , hemodialysis , discovery and development of direct thrombin inhibitors , anticoagulant , heparin induced thrombocytopenia , platelet , platelet factor 4 , thrombosis , platelet activation , pharmacology , thrombin , immunology , percutaneous coronary intervention , myocardial infarction
Awareness is increasing concerning the development of antibodies to heparin–platelet factor 4 complex in both regular hemodialysis patients and those treated with continuous forms of renal replacement therapy. Although the development of antibodies does not result in thrombocytopenia or thrombosis in some patients, most patients present with thrombocytopenia, premature platelet activation, and clotting of the extracorporeal circuit. When systemic anticoagulation is also required to treat venous thrombosis, then synthetic heparinoids or recombinant hirudin will be the agents of choice. However, neither the synthetic heparinoids nor hirudin are without problems. A few patients may have cross‐reacting antibodies against the currently available heparinoids. Similarly, antibodies may develop against recombinant hirudin, leading to a potentiation of anticoagulant activity and increased risk of hemorrhage. In the future, thrombin inhibitors such as recombinant hirudin and the arginine derivative argatroban will probably be the agents most widely used to prevent thromboembolic complications. However, anti‐platelet agents used alone or in combination with hirudin or synthetic heparinoids may provide adequate treatment by inhibiting both platelet and clotting cascade activation.