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Heparin‐induced thrombocytopenia during renal replacement therapy
Author(s) -
Davenport Andrew
Publication year - 2004
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/j.1492-7535.2004.01108.x
Subject(s) - medicine , argatroban , heparin , heparin induced thrombocytopenia , hemodialysis , hirudin , renal replacement therapy , thrombosis , venous thrombosis , discovery and development of direct thrombin inhibitors , platelet factor 4 , direct thrombin inhibitor , anticoagulant , dialysis , bivalirudin , platelet , warfarin , thrombin , dabigatran , atrial fibrillation , percutaneous coronary intervention , myocardial infarction
There is increasing awareness that antibodies to heparin/platelet factor 4 complex can develop in both those with acute renal failure treated with continuous forms of renal replacement therapy and, to a lesser extent, regular hemodialysis patients. Clinical manifestations include premature clotting of the extracorporeal circuit and increased central venous thrombosis with indwelling venous dialysis catheters, associated with thrombocytopenia and increased platelet activation. Nevertheless, a minority of patients who develop heparin/platelet factor 4 antibodies do not have thrombocytopenia or thrombosis. When systemic anticoagulation is also required to treat venous thrombosis, then synthetic heparinoids or the direct thrombin inhibitors argatroban or recombinant hirudins are the agents of choice. Neither the synthetic heparinoids nor hirudin, however, are without their own problems, in that a minority of patients may have cross‐reacting antibodies against the currently available heparinoids, and antibodies may similarly develop against recombinant hirudin, in this case leading to a potentiation of anticoagulant activity and increased risk of hemorrhage.