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4Key words:maintenance hemodialysis, platelet thrombus, cold stimulus, heparin, heating in the circuit 〈Abstract〉 Pale yellow granules start to adhere in the dialysis circuit immediately after hemodialysis initiation, and coagulate the circuit in some cases. This frequently occurs in winter, and is avoided by warming the dialysis circuit to 37℃ at the time of priming. We investigated the granules and cause of their formation. On electron microscopy, the granules were platelet thrombi formed by activated platelets. There were no common findings in the past medical history of dialysis or primary disease and no common symptom other than coagulation of the circuit among 5 cases. No cryoglobulinemia nor cold agglutinin disease related to cold stimulation was noted, and all antibodies related to heparin-induced thrombocytopenia were negative. Compared to non-granule-forming dialysis patients, no difference was noted on blood testing, and the platelet count was within the normal range, but the rate of heparin-induced reduction of the mean platelet volume(MPV)was greater(p=0.016). An increase in the non-fractionated heparin dose did not influence granule formation, but warming of the dialysis circuit at the time of priming and switch of the anticoagulant to low-molecular-weight heparin or nafamostat inhibited granule formation and avoided coagulation of the circuit. This pathology is similar to thrombocytopenia in patients under systemic heparinization in hypothermic surgery, suggesting that cold stimulation in the dialysis circuit and the macromolecular heparin fraction are involved in pale yellow granule formation.
4Key words:maintenance hemodialysis, platelet thrombus, cold stimulus, heparin, heating in the circuit 〈Abstract〉 Pale yellow granules start to adhere in the dialysis circuit immediately after hemodialysis initiation, and coagulate the circuit in some cases. This frequently occurs in winter, and is avoided by warming the dialysis circuit to 37℃ at the time of priming. We investigated the granules and cause of their formation. On electron microscopy, the granules were platelet thrombi formed by activated platelets. There were no common findings in the past medical history of dialysis or primary disease and no common symptom other than coagulation of the circuit among 5 cases. No cryoglobulinemia nor cold agglutinin disease related to cold stimulation was noted, and all antibodies related to heparin-induced thrombocytopenia were negative. Compared to non-granule-forming dialysis patients, no difference was noted on blood testing, and the platelet count was within the normal range, but the rate of heparin-induced reduction of the mean platelet volume(MPV)was greater(p=0.016). An increase in the non-fractionated heparin dose did not influence granule formation, but warming of the dialysis circuit at the time of priming and switch of the anticoagulant to low-molecular-weight heparin or nafamostat inhibited granule formation and avoided coagulation of the circuit. This pathology is similar to thrombocytopenia in patients under systemic heparinization in hypothermic surgery, suggesting that cold stimulation in the dialysis circuit and the macromolecular heparin fraction are involved in pale yellow granule formation.
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