title: Continuous venovenous haemofiltration using polyacrylonitrile filters does not activate contact system and intrinsic coagulation pathways.
abstract: OBJECTIVE
  To investigate whether continuous venovenous haemofiltration using polyacrylonitrile filters causes activation of the contact system and intrinsic coagulation pathways and if this, and/or low plasma levels of endogenous anticoagulants, influences filter lifespan.
  
  
  METHODS
  Observational study.
  
  
  METHODS
  University Teaching Hospital Intensive Care Unit.
  
  
  METHODS
  Twelve critically ill patients with acute renal failure receiving continuous venovenous haemofiltration.
  
  
  METHODS
  Blood samples were taken before starting haemofiltration, at 15 min, 1 h, 3-4 h, 8-12 h, 24 h and at 24-h intervals thereafter until filter blockage occurred. Measurement was made of the contact and intrinsic coagulation system proteins factor XII, activated factor XII and prekallikrein and the protease inhibitors antithrombin III, heparin co-factor II, alpha 2-macroglobulin and C1-esterase inhibitor. Thrombin-antithrombin complex levels were measured to provide evidence of thrombin generation.
  
  
  RESULTS
  (i) Factor XII, prekallikrein and contact system inhibitors were subnormal in 10/12 and activated factor XII raised in 11/12 patients at baseline, implying pre-existing contact pathway activation. (ii) No change occurred during haemofiltration in the intrinsic coagulation pathway factor or inhibitor levels. (iii) Clotting of the filter circuit within the first 24 h occurred in 5/12 and was associated with low baseline levels of antithrombin III and heparin co-factor II. Only in these patients did thrombin-antithrombin complex levels rise significantly.
  
  
  CONCLUSIONS
  The contact system was not activated further by continuous venovenous haemofiltration using polyacrylonitrile filters in critically ill patients. Premature clotting of the haemofilter circuit was more common in patients with very low levels of antithrombin III and heparin co-factor II; although this was related to thrombin generation, the intrinsic coagulation pathway does not appear to be implicated.
authors.affiliation: Bloomsbury Institute of Intensive Care Medicine, Department of Medicine, University College London Medical School, UK.
authors.forename: J
authors.initials: J
authors.lastname: Salmon
authors.forename: R
authors.initials: R
authors.lastname: Cardigan
authors.forename: I
authors.initials: I
authors.lastname: Mackie
authors.forename: S L
authors.initials: SL
authors.lastname: Cohen
authors.forename: S
authors.initials: S
authors.lastname: Machin
authors.forename: M
authors.initials: M
authors.lastname: Singer
mesh_terms: D000180:Acrylic Resins; D058186:Acute Kidney Injury / Q000628:therapy*; D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D000990:Antithrombin III / Q000032:analysis; D001777:Blood Coagulation; D016638:Critical Illness; D005174:Factor XII / Q000032:analysis; D005260:Female; D006440:Hemofiltration / Q000379:methods*; D006801:Humans; D008297:Male; D008567:Membranes, Artificial; D008875:Middle Aged; D010447:Peptide Hydrolases / Q000032:analysis; D010865:Pilot Projects; D011288:Prekallikrein / Q000032:analysis; D011480:Protease Inhibitors / Q000032:analysis
chemical_list: D000180:Acrylic Resins; D008567:Membranes, Artificial; D011480:Protease Inhibitors; C046193:antithrombin III-protease complex; C010504:polyacrylonitrile; D000990:Antithrombin III; D005174:Factor XII; D011288:Prekallikrein; D010447:Peptide Hydrolases