Hypercoagulable states and antithrombotic strategies in recurrent vascular access site thrombosis.
Vascular access site thrombosis is a major cause of morbidity in patients receiving hemodialysis. The role of hypercoagulable states in recurrent vascular access site thrombosis remains poorly understood. Data are limited regarding systemic anticoagulation to improve access graft patency, because of concern about hemorrhagic complications. We determined the prevalence of hypercoagulable states and clinical outcome (thrombotic and hemorrhagic) after initiation of antithrombotic therapy in a series of patients with recurrent vascular access site thrombosis. We evaluated 31 patients who had sustained 119 thrombotic events that resulted in vascular access graft failure during the year before evaluation. Sixty-eight percent of patients tested had elevated concentrations of antibody to anticardiolipin or topical bovine thrombin, and 18% of patients tested had heparin-induced antibodies. More than 90% of patients had elevated factor VIII concentration, 62% had elevated fibrinogen concentrations, and 42% had elevated C-reactive protein concentrations. Twenty-nine patients were given antithrombotic therapy: 13 with warfarin sodium, 12 with unfractionated heparin (UFH), and 11 with low molecular weight heparin (LMWH). Seven patients received more than one antithrombotic agent, sequentially. Nineteen patients have had no thrombotic events since beginning antithrombotic therapy (10 with warfarin, 3 with UFH, 6 with LMWH). Mean follow-up was 8.6 months (median, 7 months). Eight patients sustained 10 bleeding complications (5 with warfarin, 3 with UFH, and 2 with LMWH). In conclusion, hypercoagulable states are common in patients with recurrent vascular access site thrombosis. Antithrombotic therapy may increase vascular access graft patency, but is associated with significant risk for hemorrhage. Prospective studies are needed to evaluate the role and safety of antithrombotic agents in improving vascular access graft patency.
O'shea
Susan I
SI
Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA. oshea005@mc.duke.edu
Lawson
Jeffrey H
JH
Reddan
Donal
D
Murphy
Michael
M
Ortel
Thomas L
TL
D000328:Adult; D000368:Aged; D017153:Antibodies, Anticardiolipin / Q000032:analysis; D001166:Arteriovenous Shunt, Surgical / Q000009:adverse effects / Q000379:methods; D015415:Biomarkers / Q000032:analysis; D002097:C-Reactive Protein / Q000032:analysis; D002408:Catheters, Indwelling / Q000009:adverse effects*; D005169:Factor VIII / Q000032:analysis; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006083:Graft Occlusion, Vascular / Q000188:drug therapy / Q000209:etiology; D006801:Humans; D007676:Kidney Failure, Chronic / Q000628:therapy; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D012008:Recurrence; D006435:Renal Dialysis / Q000009:adverse effects* / Q000295:instrumentation; D018570:Risk Assessment; D013927:Thrombosis / Q000175:diagnosis / Q000188:drug therapy / Q000209:etiology*; D016896:Treatment Outcome; D014859:Warfarin / Q000627:therapeutic use
D017153:Antibodies, Anticardiolipin; D015415:Biomarkers; D005343:Fibrinolytic Agents; D014859:Warfarin; D005169:Factor VIII; D002097:C-Reactive Protein