Heparininduzierte Thrombozytopenie bei dialysepflichtiger Niereninsuffizienz

Heparin-induced thrombocytopenia (HIT) is a rare but serious complication of the administration of unfractionated heparin (UFH). Low molecular weight heparins (LMWH) may also cause HIT. Immunization against the heparin-platelet factor 4 complex induces a strong platelet activation leading to a ≥50% decline of the platelet count frequently accompanied by venous and arterial thromboembolisms. The HIT can be divided into five phases. Whereas in orthopedic surgery HIT no longer plays a role, mostly due to LMWH and direct oral anticoagulants (DOAC), it remains an important diagnosis in patients with dialysis-dependent kidney failure affecting 0.25–1%, mostly during initiation of hemodialysis treatment. The diagnosis of HIT has a tremendous impact on dialysis patients, as UFH or LMWH may have to be avoided for many years. If HIT is clinically suspected, UFH and LMWH should immediately be stopped and an alternative therapeutic anticoagulation, primarily with argatroban, should be initiated. Danaparoid or bivalirudin (off label) may also be used. A negative HIT-immunoglobulin G (IgG) enzyme-linked immunosorbent assay (ELISA) excludes HIT, a positive heparin-induced platelet activation (HIPA) test confirms it. If HIT is complicated by thromboembolisms (HITT), the therapeutic anticoagulation should be continued for at least 3 months. Vitamin K antagonists are no longer clearly preferred in dialysis patients. The DAOCs apixaban or rivaroxaban seem to be reasonable options (off label). In isolated HIT anticoagulation can be terminated after a maximum of 4 weeks. For anticoagulation during dialysis regional citrate anticoagulation, argatroban and fondaparinux (off label) are suitable choices.