Tranexamic acid inhibits fibrinolysis, shortens the bleeding time and improves platelet function in patients with chronic renal failure

Background: A defect in platelet function is the main determinant of the pr olonged bleeding time in chronic renal failure (CRF). We previously reporte d a significant correlation between platelet abnormalities and elevated pla sma markers of plasmin and thrombin generation. Our aim was to explore thr effect of inhibiting both plasmin action with tranexamic acid (TA) and thro mbin production with low molecular weight heparin (LMWH), on the bleeding t ime (BT) and platelet function in patients with CRF. Methods: 37 patients w ith CRF (mean creatinine 8.6 +/- 4.4 mg/dl) under conservative treatment, w ith prolonged BT, entered this study and received TA during 6 days, with (n = 24) and without LMWH (n = 13). BT, platelet aggregation/secretion, plate let granule contents, von Willebrand factor and parameters of coagulation a nd fibrinolysis were recorded before and at the end of treatment. Results: The BT was shortened in 26/37 (67%) patients. This effect was associated wi th significant improvement of platelet aggregation and secretion, with decr ease to a normal range of fibrin/fibrinogen degradation products, mild incr ease in plasmin-antiplasmin complexes and pronounced reduction of circulati ng plasminogen. No differences were seen among patients with or without LMW H. No serious side effects or complications were observed. Interpretation: These findings indicate that the activation of fibrinolysis plays a signifi cant role in the defect of primary hemostasis in patients with CRF. inhibit ion of plasmin activity with TA shortens the BT and improves platelet funct ion in the majority of patients with severe disease.