Putative novel mediators of acute kidney injury in critically ill patients: handling by continuous venovenous haemofiltration and effect of anticoagulation modalities

Introduction: Novel putative mediators of acute kidney injury (AKI) include immune-cell derived tumour necrosis factor-like weak inducer of apoptosis (TWEAK), angiopoietin-2 (Ang-2) and protein pentraxin-3 (PTX3). The effect of continuous venovenous heamofiltration (CVVH) and different anticoagulation regimens on plasma levels were studied. Methods: At 0, 10, 60, 180 and 720 minutes of CVVH, samples were collected from preand postfilter blood and ultrafiltrate. No anticoagulation (n=13), unfractionated heparin (n=8) or trisodium citrate (n=21) were compared. Results: Concentrations of TWEAK, Ang-2 and PTX3 were hardly affected by CVVH since the mediators were not (TWEAK, PTX3) or hardly (Ang-2) detectable in ultrafiltrate, indicating negligible clearance by the filter in spite of molecular sizes (TWEAK, PTX3) at or below the cutoff of the membrane. Heparin use, however, was associated with an increase in inand outlet plasma TWEAK. Conclusion: Novel AKI mediators are not cleared nor produced by CVVH. However, heparin anticoagulation increased TWEAK levels in patient’s plasma whereas citrate did not, favouring the latter as anticoagulant in CVVH for AKI. Schilder.indd 126 19-8-2015 10:52:57 127 Levels of putative novel mediators of AKI and influence of anticoagulation and CVVH