Research
Tirofiban preserves platelet loss during continuous renal replacement therapy in a randomised prospective open-blinded pilot study
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* Corresponding author: Andreas Link link@med-in.uni-saarland.de
1 Klinik für Innere Medizin III, Universitätsklinikum des Saarlandes, Kirrberger Strasse, 66421 Homburg/Saar, Germany
2 Klinik für Innere Medizin IV, Universitätsklinikum des Saarlandes, Kirrberger Strasse, 66421 Homburg/Saar, Germany
Critical Care 2008, 12:R111 doi:10.1186/cc6998
See related commentary by Storm and Jörres, http://ccforum.com/content/12/6/193
Published: 29 August 2008Abstract
Introduction
Approximately one third of all patients with cardiogenic shock suffer from acute kidney injury. Percutaneous coronary intervention, intra-aortic balloon pump, and continuous renal replacement therapy (CRRT) require effective antiplatelet therapy and anticoagulation, resulting in a high risk for platelet loss and bleeding events. The reversible platelet glycoprotein IIb/IIIa receptor inhibitor tirofiban was investigated to preserve platelet number and activation in a prospective open-blinded endpoint evaluation study.
Methods
Forty patients with cardiogenic shock and acute kidney injury requiring CRRT were randomly assigned to two groups receiving unfractioned heparin (UFH) (n = 20) or a combined anticoagulation with UFH and tirofiban (n = 20). The primary endpoint was platelet loss during CRRT. Secondary endpoints were urea reduction, haemofilter life span, bleeding events, and necessity for platelet transfusions.
Results
In UFH-treated patients, the percentage of platelet-monocyte aggregates significantly increased (P < 0.001) and consecutively platelet cell count significantly decreased (P < 0.001). In contrast, combined treatment with UFH and tirofiban significantly decreased platelet-monocyte aggregates and platelet numbers (P < 0.001).
Conclusions
This pilot study provides evidence that the use of tirofiban in addition to UFH prevents platelet loss and preserves platelet function in patients with cardiogenic shock and acute kidney injury requiring CRRT. The pathophysiological inhibition of platelet aggregation and platelet-monocyte interaction appears to be causally involved.