Clotting of the extracorporeal circuit, with a corresponding loss of blood in the circuit remains the Achilles heel of continuous renal replacement therapies (CRRT) [1]. Pre-mature circuit clotting results not only in a loss of efficacy of treatment, but also an increase in nursing work load, and higher financial costs due to circuit replacement [2, 3].Early circuit clotting may be the consequence of numerous factors including bio-incompatibility, inadequate vascular access, and critical illness in general (including thrombin generation, thrombocytosis, blood transfusions etc.) [4][5][6][7][8], along with specific CRRT circuitrelated factors such as stasis of blood flow [7, 9], hemoconcentration [7], and blood-air contact in air-detection chambers [7].Hypothermia has long been known to affect coagulation [10, 11] and therapeutic hypothermia may useful for reducing the risk of thrombus formation [12]. These observations are further supported by data showing a reduced pro-coagulant response to recombinant activated factor VII when administered in severe hypothermia [13][14][15].Based on these observations, Krouzecky and colleagues now report on the deliberate cooling of blood in the extracorporeal CRRT circuit down to a temperature of 20°C as a novel technique for regional anticoagulation in an experimental porcine model [16]. This study randomized 12 anesthetized and ventilated pigs to 6 h of CRRT (neutral fluid balance, 20 mL/kg per h) with either regional blood cooling of the extracorporeal circuit (hypothermic circuit) or control (isothermic circuit). No anticoagulation was used. Regional temperature manipulation in the extracorporeal circuit was achieved by use of a cooling exchange device at the blood inflow tract (set at 20°C) and a concomitant warming exchange device at the blood return tract (set at 38°C), both of which were monitored and controlled by a central computer. Numerous parameters related to circuit patency (i.e. time to clotting, alarm-trigger pump stopping, transmembrane pressure) and coagulation status [i.e. thrombin-antithrombin complexes (TAT), thromboelastography (TEG)] were determined before, during and following the prescribed therapy. The authors also investigated whether regional blood cooling altered systemic hemodynamics or induced significant hemolysis compared with isothermic controls. The key finding of the study was that regional blood cooling was associated with patency of all the extracorporeal circuits for the duration of applied CRRT, whereas five of the six isothermic circuits prematurely clotted. The clotting in the isothermic circuits was associated with a significant increase in transmembrane pressures and an increase in detectable extracorporeal TAT complexes, compared to the hypothermic circuits. In addition, blood sampling from the hypothermic circuits showed evidence of a significant delay in clotting time and a decrease clotting rate when assessed by standardized TEG, a functional assay of clot formation and lysis.