Thromb Haemost 2005; 94(06): 1245-1250
DOI: 10.1160/TH05-02-0123
Platelets and Blood Cells
Schattauer GmbH

The effect of long term, low-dose tranexamic acid treatment on platelet dysfunction and haemoglobin levels in haemodialysis patients

Mišo Šaboviã
1   Department of Vascular Diseases, University Medical Centre, Ljubljana, Slovenia
,
Irena Preložnik Zupan
2   Department of Haematology, University Medical Centre, Ljubljana, Slovenia
,
Barbara Salobir
1   Department of Vascular Diseases, University Medical Centre, Ljubljana, Slovenia
,
Igor Zupan
3   Department of Cardiology, University Medical Centre, Ljubljana, Slovenia
,
Peter Černelã
2   Department of Haematology, University Medical Centre, Ljubljana, Slovenia
,
Janez Lavre
4   Department of Nephrology and Dialysis, Slovenj Gradec General Hospital, Slovenia
,
Bojan Vujkovac
4   Department of Nephrology and Dialysis, Slovenj Gradec General Hospital, Slovenia
› Author Affiliations
Further Information

Publication History

Received 20 February 2005

Accepted after resubmission 05 September 2005

Publication Date:
07 December 2017 (online)

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Summary

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.