in a recent article for critical care link and colleagues reported that the reversible platelet glycoprotein iib / iiia antagonist tirofiban may prevent platelet activation and preserves platelet numbers during continuous venovenous haemodialysis in patients with cardiogenic shock .
acute kidney failure is a frequent complication in the critically ill , particularly so in patients with severe sepsis / septic shock or with acute myocardial infarction / cardiogenic shock .
often this complication will entail the need for renal replacement therapy until kidney function recovers .
contact of blood with artificial surfaces of extracorporeal systems , however , may lead to platelet activation , to formation of platelet  monocyte aggregates , and to induction of inflammation . in the majority of cases ,
extracorporeal therapy thus requires an effective anticoagulation strategy that , in turn , may put the patient at risk of bleeding complications . especially during continuous renal replacement therapy ( crrt ) ,
platelet dysfunction may occur with increased activation and aggregation and  ultimately  with platelet loss . in recent years
, glycoprotein iib / iiia antagonists have found their way into clinical routine , serving as powerful receptor blockers in the final stage of platelet activation ; for example , in patients with acute coronary syndromes and percutaneous transluminal angioplasty [ 4 - 6 ] . these antagonists have also been proposed as a pharmacological strategy to prevent platelet loss during extracorporeal circulation , especially in cardiac surgery ( platelet anaesthesia ) ; however , their potential role in extracorporeal renal replacement therapies is unclear at present . in their pilot study link and
colleagues randomly assigned 40 patients with cardiogenic shock and acute kidney failure requiring crrt to two groups , either receiving unfractionated heparin ( ufh ) ( n = 20 ) or receiving a combined anticoagulation with ufh and tirofiban ( n = 20 ) .
they found in the group receiving only ufh that the percentage of platelet  monocyte aggregates was significantly increased ( p < 0.001 ) and the platelet number was significantly decreased ( p < 0.001 ) . in contrast , platelet  monocyte aggregates and the decrement in platelet numbers were significantly reduced under combined therapy ( p < 0.001 ) .
there were no significant differences between the groups regarding the efficacy of crrt , the haemofilter lifespan , or bleeding events .
platelet transfusions were only necessary in three patients of the ufh group ( p = 0.016 ) .
the authors conclude that , in patients with cardiogenic shock and acute kidney injury requiring crrt , the use of tirofiban in addition to ufh prevents platelet loss and platelet  monocyte interaction and may preserve platelet function .
whilst these findings are of interest and are of potential clinical relevance , caution needs to be exercised in their interpretation . as is also reflected in the present study , patients with acute coronary syndromes and cardiogenic shock
will often be subjected to a variety of specific ( pharmacological and nonpharmacological ) interventions that may impact on platelet function and/or number .
this includes the administration of anticoagulants ( heparins , heparinoids , thrombin inhibitors ) , antiplatelet agents ( glycoprotein iib / iiia antagonists , acetylsalicylic acid , thienopyridine ) , and catecholamines , as well as treatment with intraaortic counterpulsation . in a fairly small and heterogeneous cohort
the same holds true for the potential influence of the type and mode of the extracorporeal treatment and materials , and , last but not least , for the metabolic control / uraemic state of the patient .
moreover , the response of individual patients to acetylsalicylic acid and/or thienopyridin may vary considerably up to the point of the new and not completely understood phenomenon of thienopyridine nonresponders , an issue that will also have to be carefully considered in a subsequent study .
the platelet numbers in the ufh therapy group were more than halved , dropping from an average of ( 216  64.3 )  10/l to as low as ( 87.3  41.1 )  10/l within 4 days  three patients with platelet counts < 20  10/l even requiring platelet transfusions .
given the fact that the authors used modern polysulphone capillary haemofilters and employed a continuous venovenous haemodialysis regime that reduces transmembrane pressures and thus reduces shear stress compared with postdilution continuous venovenous haemofiltration , the observed extent of platelet loss seems unusually large and remains unexplained . in summary , the study by link and colleagues raises the important question of whether platelet anaesthesia with tirofiban prevents platelet activation and loss during crrt .
the data presented indicate a significantly reduced platelet loss with additional glycoprotein iib / iiia antagonist therapy compared with ufh therapy alone . owing to the small sample size
, however , the potential impact of additional treatment variables could not be clarified . a substantially larger , adequately powered study
 link and colleagues present a pilot study investigating platelet function and platelet numbers in patients with cardiogenic shock and acute kidney failure undergoing continuous venovenous haemodialysis . 
 their data indicate a significantly reduced platelet loss with combined therapy of unfractionated heparin plus tirofiban , the glycoprotein iib / iiia antagonist , compared with unfractionated heparin therapy alone . owing to the small sample size , however , the potential impact of additional treatment variables ( antiplatelet agents , intraaortic counterpulsation ) could not be clarified . a substantially larger , adequately powered study 
 is therefore called for to establish the potential clinical relevance of these findings . 
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