title: The effect of long-term, low-dose tranexamic acid treatment on platelet dysfunction and haemoglobin levels in haemodialysis patients.
abstract: Some previous studies suggest that activation of the fibrinolytic system may induce platelet dysfunction in haemodialysis patients. Accordingly, inhibition of fibrinolysis may improve platelet dysfunction, and speculatively increase haemoglobin levels. We tested this hypothesis. The study group comprised 22 patients (14 male, 8 female, median age 62), who had been on maintenance haemodialysis for more than one year. Patients were treated for three months with low-dose tranexamic acid (TXA), a potent anti-fibrinolytic agent. The dosages of erythropoietin and the haemodialysis procedure were not changed significantly during the study. We primarily followed platelet function (by in vitro closure time test) and haemoglobin values. Patients were divided into those with substantially prolonged (N = 9) and those with slightly delayed or normal (N = 13) in vitro closure time. Treatment with TXA resulted in a significant improvement of platelet function and increased levels of haemoglobin in the first group, and no changes in either platelet function or haemoglobin values in the second group. TXA in the dosage used was biologically active, since a significant decrease in plasminogen and D-dimer were found in both groups. No significant changes in other fibrinolytic parameters or von Willebrand factor were found. No complications in terms of arterial or venous thrombosis were observed. Our pilot study suggests that long-term, low-dose TXA treatment of haemodialysis patients with substantially prolonged in vitro closure time results in a significant improvement of platelet dysfunction and a significant increase in haemoglobin values. These new, promising results merit further investigation in larger studies.
authors.affiliation: Department of Vascular Diseases University Medical Centre, Zaloska 2, 1000 Ljubljana, Slovenia. miso.sabovic@trnovo.kclj.si
authors.forename: Miso
authors.initials: M
authors.lastname: Sabovic
authors.forename: Irena Preloznik
authors.initials: IP
authors.lastname: Zupan
authors.forename: Barbara
authors.initials: B
authors.lastname: Salobir
authors.forename: Igor
authors.initials: I
authors.lastname: Zupan
authors.forename: Peter
authors.initials: P
authors.lastname: Cernelc
authors.forename: Janez
authors.initials: J
authors.lastname: Lavre
authors.forename: Bojan
authors.initials: B
authors.lastname: Vujkovac
mesh_terms: D000368:Aged; D000933:Antifibrinolytic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D001792:Blood Platelets / Q000187:drug effects*; D004921:Erythropoietin / Q000008:administration & dosage / Q000627:therapeutic use; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005342:Fibrinolysis / Q000187:drug effects; D006454:Hemoglobins / Q000378:metabolism; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000628:therapy; D008297:Male; D008875:Middle Aged; D010958:Plasminogen / Q000378:metabolism; D010979:Platelet Function Tests; D011446:Prospective Studies; D006435:Renal Dialysis; D013997:Time Factors; D014148:Tranexamic Acid / Q000008:administration & dosage / Q000627:therapeutic use*
chemical_list: D000933:Antifibrinolytic Agents; D005338:Fibrin Fibrinogen Degradation Products; D006454:Hemoglobins; C036309:fibrin fragment D; D004921:Erythropoietin; D014148:Tranexamic Acid; D010958:Plasminogen