Evaluation of Circuit and AV Fistula Clotting and Detection of Anti-PF4/Heparin Complex Antibodies in Hemodialysis Patients Suspected of Having Heparin-Induced Thrombocytopenia

• Published in: Clinical and applied thrombosis/hemostasis Vol. 19; no. 1; pp. 73 - 78
• Main Authors: Matsuo, Takefumi, Wanaka, Keiko, Walenga, Jeanine M.
• Format: Journal Article
• Language: English
• Published: Los Angeles, CA SAGE Publications 01.01.2013; SAGE PUBLICATIONS, INC
• Subjects: Aged; Aged, 80 and over; Anastomosis, Surgical; Anticoagulants; Anticoagulants - administration & dosage; Anticoagulants - adverse effects; Autoantibodies - blood; Blood clots; Female; Fistula; Hemodialysis; Heparin - administration & dosage; Heparin - adverse effects; Humans; Immunoglobulins; Male; Middle Aged; Platelet Count; Platelet Factor 4; Renal Dialysis; Retrospective Studies; Thrombocytopenia - blood; Thrombocytopenia - chemically induced; Thrombocytopenia - complications; Thrombosis; Thrombosis - blood; Thrombosis - etiology; Time Factors; hemodialysis; circuit clotting; anti-PF4/heparin complex antibodies; arteriovenous fistula thrombosis; heparin-induced thrombocytopenia
• ISSN: 1076-0296; 1938-2723
• DOI: 10.1177/1076029612436676

A retrospective study was performed to elucidate the characteristics of heparin-induced thrombocytopenia (HIT) in newly treated hemodialysis (HD) patients who essentially required anticoagulation with unfractionated heparin (UFH). Seventy-eight patients suspected of having HIT within 3 months of starting HD with UFH were selected for this study. Their platelet counts were routinely followed, and anti-PF4/heparin complex antibodies (HIT antibodies) were measured with enzyme-linked immunosorbent assay (ELISA) until the titer became negative. The characteristics of thrombocytopenia were a platelet count of ≤150 × 109/L and/or decrease of ≥30% and as caused by the intermittent use (3 times/a week) of UFH during HD. Fifty-five patients showed unexpected clotting in the extracorporeal circuit and/or arteriovenous fistula (AVF) thrombosis, while 23 patients had neither of these complications. The patients were classified into HD-related and non-HD-related thrombus groups. The impact of various combinations of the 3 clinical factors (thrombocytopenia, timing, and HD-related thrombus) and the results of ELISA as a laboratory factor were examined. A combination of 2 platelet factors (thrombocytopenia and timing) and ELISA positivity did not reveal the presence of HIT, while a combination of the 3 clinical factors and a positive ELISA improved the accuracy of HIT diagnosis. The findings on the 4-factor combination were supported by high rates of seroconversion in a serotonin release assay. Combining appropriate clinical factors and a positive ELISA may lead to the proper management of HD patients suspected of having HIT. In conclusion, while HD patients showed a drop of ≤150 × 109/L or ≥30% on days 7 to 30, unexpected clotting in the circuit and/or AVF thrombosis was considered as a sign of HIT development.