65, P = 0.02), and not with PTT, anti-Xa, F1+2, TAT selleck SB203580 and D-dimers.Arterial anti-Xa at t1 and t2 (one hour after the nadroparin bolus) correlated with antithrombin (R = 0.54, P = 0.048 and R = 0.48, P = 0.08). Anti-Xa activity was not related to body weight. There was a positive correlation between arterial antithrombin and ETPCmax at t1 and t2 (R = 57, P = 0.03 and R = 0.79, P = 0.001) and ETPAUC at t1 and t2 (R = 0.46, P = 0.10 and R = 0.41, P = 0.14). ETP and anti-Xa correlated negatively if all samples were taken together (R = -0.36, P = 0.001).Relation between markers of coagulation, severity of organ failure and circuit lifeMedian circuit life was 24.5 hours (IQR 12 to 37 hours). Short circuit life was defined as 12 hours of less (the lower quartile).

At baseline, patients with short circuit life had a longer PTT, aPTT, higher TAT and lower ETP. They also had higher SOFA scores (Table (Table3).3). During CVVH and nadroparin infusion, anti-Xa and platelets were significantly lower in patients with short circuit life, PTT, aPTT, TAT and D-dimers were significantly longer or higher and ETP was slower and depressed (Table (Table33).Table 3Comparison of baseline markers of coagulation and severity of organ failure between patients with circuit life of 12 hours or less (lower quartile) and those with circuit life more than 12 hoursMedian SOFA score was 10. Patients with high SOFA score (>10) had longer PTT, aPTT, a depressed ETP, high TAT and D-dimers and a significantly shorter circuit life. During CVVH anti-Xa was lower and postfilter ETP was slow and depressed (Table (Table44).

Table 4Comparison of baseline markers of coagulation and circuit life between patients with SOFA score of 10 or less (median) and those with SOFA score of more than 10DiscussionThis randomized cross-over study in critically ill patients with AKI compared the hemostasis during anticoagulation with the LMWH nadroparin between two doses of CVVH using a cellulose tri-acetate filter. We found no signs of accumulation of anticoagulant activity in arterial blood and no signs of removal by filtration. Anticoagulant activity was quantified by anti-Xa activity. In arterial blood, anti-Xa levels peaked upon the intravenous nadroparin bolus and gradually declined thereafter despite the continuous infusion of the LMWH in the circuit, while postfilter anti-Xa activity remained constant.

Anti-Xa activity was not detected in the ultrafiltrate.It should be noted that we did not measure nadroparin concentration but its anticoagulant activity. If hemofiltration would remove the drug we would expect higher drug concentrations in group 1 with Anacetrapib the lower CVVH, and assuming a linear relation between dose and effect, also a higher anti-Xa activity. The opposite was the case. Differences in anti-Xa activity between groups can therefore not be explained by a different handling of nadroparin by filtration.