Email updates

Keep up to date with the latest news and content from Critical Care and BioMed Central.

Open Access Highly Accessed Research

Tirofiban preserves platelet loss during continuous renal replacement therapy in a randomised prospective open-blinded pilot study

Andreas Link1*, Matthias Girndt2, Simina Selejan1, Ranja Rbah1 and Michael Böhm1

Author Affiliations

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

For all author emails, please log on.

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 2008

Abstract

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.