title: Putative novel mediators of acute kidney injury in critically ill patients: handling by continuous venovenous hemofiltration and effect of anticoagulation modalities.
abstract: BACKGROUND
  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 hemofiltration (CVVH) and different anticoagulation regimens on plasma levels were studied.
  
  
  METHODS
  At 0, 10, 60, 180 and 720 min of CVVH, samples were collected from pre- and 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 in- and outlet plasma TWEAK.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Nephrology, VU University medical center, De Boelelaan 1117, 1081, HV, Amsterdam, The Netherlands. louiseschilder@hotmail.com.
authors.forename: Louise
authors.initials: L
authors.lastname: Schilder
authors.affiliation: Department of Nephrology, VU University medical center, De Boelelaan 1117, 1081, HV, Amsterdam, The Netherlands. sa.nurmohamed@vumc.nl.
authors.forename: S Azam
authors.initials: SA
authors.lastname: Nurmohamed
authors.affiliation: Department of Nephrology, VU University medical center, De Boelelaan 1117, 1081, HV, Amsterdam, The Netherlands. pm.terwee@vumc.nl.
authors.forename: Pieter M
authors.initials: PM
authors.lastname: ter Wee
authors.affiliation: Department of Molecular Cell Biology and Immunology, Netherlands, The Netherlands. nj.paauw@vumc.nl.
authors.forename: Nanne J
authors.initials: NJ
authors.lastname: Paauw
authors.affiliation: Department of Intensive Care, VU University Medical Center, Amsterdam, The Netherlands. arj.girbes@vumc.nl.
authors.forename: Armand R J
authors.initials: AR
authors.lastname: Girbes
authors.affiliation: Department of Intensive Care, Medisch Spectrum Twente, Enschede, The Netherlands. beishuizen@vumc.nl.
authors.forename: Albertus
authors.initials: A
authors.lastname: Beishuizen
authors.affiliation: Department of Molecular Cell Biology and Immunology, Netherlands, The Netherlands. rhj.beelen@vumc.nl.
authors.forename: Robert H J
authors.initials: RH
authors.lastname: Beelen
authors.affiliation: Department of Intensive Care, Erasmus Medical Center, Rotterdam, The Netherlands. abj.groeneveld@erasmusmc.nl.
authors.forename: A B Johan
authors.initials: AB
authors.lastname: Groeneveld
mesh_terms: D058186:Acute Kidney Injury / Q000276:immunology* / Q000628:therapy*; D000328:Adult; D000368:Aged; D000925:Anticoagulants / Q000008:administration & dosage; D003131:Combined Modality Therapy / Q000379:methods; D003422:Critical Care / Q000379:methods; D016638:Critical Illness; D004334:Drug Administration Schedule; D005260:Female; D006440:Hemofiltration / Q000379:methods*; D006493:Heparin / Q000008:administration & dosage*; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D016896:Treatment Outcome; D055815:Young Adult
chemical_list: D000925:Anticoagulants; D018836:Inflammation Mediators; D006493:Heparin