Serious bleeding in a haemodialysis patient treated with recombinant hirudin

Heparin is at present the most widely used anticoagulant for haemodialysis to prevent clotting in the extracorporal circuit. Heparin-induced thrombocytopenia (HIT) type II is a serious complication rendering the further administration of unfractioned heparin as well as low-molecular-weight heparin impossible. Even available heparinoids such as danaparoid exhibit a significant cross-reactivity with HIT antibodies in 5–10% of patients and is sometimes not suitable for anticoagulation in cases of heparin intolerance. Hirudin is a direct thrombin inhibitor which forms non-covalent complexes with thrombin. In contrast to heparin it does not require endogenous cofactors. Chronic administration of r-hirudin in haemodialysis carries the risk of accumulation since unchanged hirudin is exclusively cleared by the kidney [1]. It is not removed by haemodialysis. To avoid cumulation and bleeding complications in anuric patients dose reduction has been suggested (bolus of 0.02–0.17 mg/kg prior to each haemodialysis) followed by careful monitoring with the activated partial thromboplastin time (aPTT) [2–5].