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Immune-mediated HIT results from antibodies directed against the complex of heparin and platelet factor 4, and occurs in 1–3% of heparin-exposed patients. Its main clinical complication is the development of thrombocytopenia with or without thrombosis.581 In patients with AKI undergoing CRRT, the diagnosis should therefore also be suspected in patients with repeated premature filter clotting.630 The likelihood of having HIT can be predicted by the so-called 4 T score, that includes the degree of thrombocytopenia, the timing of onset of the fall in platelet count, the presence of thrombosis or acute systemic symptoms, and the presence of other etiologies of thrombocytopenia.631 If HIT is likely, all heparins have to be stopped, including any ‘‘heparin lock’’ solutions for dialysis or other catheters.
With regard to the diagnosis and management of HIT, we refer to the recent guideline of the ACCP581 and the European best practice guideline on chronic dialysis.587 These guidelines recommend the use of therapeutic doses of an alternative nonheparin anticoagulant in patients with strong suspicion of HIT. Candidates are the direct thrombin inhibitors lepirudin, argatroban, or bivaluridin, or the antithrombin-dependent Factor Xa inhibitors, danaparoid or fondaparinix. Pharmacokinetic data and dosing guidelines for these alternative anticoagulants have been published for IHD588,632 and CRRT.633
Argatroban is a direct thrombin inhibitor, is eliminated by the liver, has a short half-life, and can be monitored with aPTT.634 A recent observational study on the use of argatroban for anticoagulation during continuous dialysis in 30 patients with AKI and HIT derived a dosing equation, based on illness severity scores or by use of indocyanine green plasma clearance.635 Regional citrate anticoagulation has been used along with reduced doses of argatroban or other nonheparin anticoagulants in cases where bleeding occurs. However, there are no published reports on this practice.
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