Recurrent Vascular Access Site Thrombosis in Patients on Hemodialysis - a Problem of Thrombophilia?.

Abstract

Abstract Introduction: Vascular access site thrombosis in patients receiving hemodialysis is a major cause of hospital admission and recurrent surgery. The underlying pathologic cause is often stenosis of the venous vessel due to fibromuscular hyperplasia. But in the case of early failure occasional studies have investigated that hypercoagulability could play an important role in this context. Aim of the study: Is there a higher prevalence of hereditary and acquired thrombophilic risk factors in patients with vascular access thrombosis in comparison to patients without? Patients: In 2002 and 2003 we examined 52 consecutive patients (mean age 66,1 years) receiving hemodialyisis. 27 patients (pts) in group 1 had a history of vascular access site thrombosis and 25 pts in group 2 had not and an open vascular access for longer than at least six months. All pts in group 1 had a history of at least two occlusions of vascular access. 10/27 pts in group 1 with prosthetic grafts had a history of thrombosis of arteriovenous fistula before implantation of PFTE graft. Methods: In every patient hereditary and acquired thrombophilic risk factors were determined including antithrombin (AT), protein C (PC), protein S (PS), factor V-G1691A-mutation (FVM), prothrombin-G20210A-mutation (FIIM), homocysteine, lipoproteine (a) (Lpa), lupus anticoagulant (LA), cardiolipin antibodies IgG and IgM (ACA), fibrinogen and factor VIII. Platelet hyperreactivity was studied by light transmittance aggregometry in platelet rich plasma (Aggregometer PAP 4, moelab inc.). Aggregation was recorded as the maximum percentage change in light transmittance from baseline using platelet poor plasma as a reference. We defined sticky platelets as platelet aggregation > 30% after induction with different concentrations of ADP (10, 1 and 0,5 μmol) in platelet rich plasma. Results: We found in 14/27 pts with vascular access site thrombosis antiphospholipd antibodies (LA and/or ACA) in comparison to only 2/25 in pts without thrombosis. Activated platelets like the sticky platelets syndrome was shown in 11/27 pts in group 1 and 4/25 pts in group 2. In both groups hyperhomocysteinaemia (23/27 pts and 21/25 resp.), factor VIII elevation (21/27 pts and 22/25 resp.), fibrinogen elevation (22/27 pts and 21/25 resp.) and high levels of Lpa (7/27 pts and 6/25 resp.) were quite similar. There were no significant differences in the number of hereditary risk factors like AT, PC, PS, FVM and FIIM in both groups. Conclusions: In patients receiving hemodialysis we found a high prevalence of acquired thrombophlic risk factors like elevation of factor VIII, homocysteine and fibrinogen. There seems to be causal relation between vascular access site thrombosis and espacially antiphospholpid antibodies and activated platelets (sticky platelets syndrome). The evaluation of these thrombophilic risk factors in patients with recurrent vascular access site thrombosis could lead to an improved antithrombotic therapy.