title: Intermittent high-permeability hemofiltration modulates inflammatory response in septic patients with multiorgan failure.
abstract: OBJECTIVE
  Continuous venovenous hemofiltration with high-permeability hemofilters is a novel approach in the adjuvant therapy of septic patients. High-permeability hemofilters are characterized by an increased pore size which facilitates the filtration of inflammatory mediators. The present study examines whether intermittent high-permeability hemofiltration has an immunomodulatory effect on polymorphonuclear leukocytes and mononuclear cells.
  
  
  METHODS
  Twenty-eight septic patients with acute renal failure were randomly allocated to either receive intermittent high-permeability or conventional hemofiltration. Intermittent high-permeability hemofiltration consisted of a daily 12-hour course of high-permeability hemofiltration alternated by conventional hemofiltration. For high-permeability hemofiltration, a newly developed high-flux polyamide membrane (P2SH) with a nominal cutoff point of 60 kD was used. For conventional hemofiltration a high-flux polyamide hemofilter (Polyflux 11S, cutoff point 30 kD) was used.
  
  
  RESULTS
  The polymorphonuclear leukocyte phagocytosis activity before starting hemofiltration was almost double the rate of healthy controls in both groups (p < 0.001). The phagocytosis rate decreased significantly during the course of intermittent high-permeability hemofiltration (p < 0.05), whereas the values remained unchanged in the conventional hemofiltration group. Incubation of high-permeability filtrates with blood from healthy donors resulted in a significant induction of phagocytosis (p < 0.001), whereas conventional filtrates had no phagocytosis-stimulating effects. In addition, incubation of healthy-donor mononuclear cells with high-permeability but not conventional filtrates resulted in a significant tumor necrosis factor alpha release (p < 0.001).
  
  
  CONCLUSIONS
  Intermittent high-permeability hemofiltration is a novel extracorporeal elimination modality which exhibits immunomodulatory effects on leukocytes, attenuating polymorphonuclear neutrophil phagocytosis. Further studies are necessary to elucidate whether these effects translate in a clinical improvement in patients suffering from sepsis.
authors.affiliation: Department of Nephrology, Charité, Humboldt University of Berlin, Berlin, Germany. stanislao.morgera@charite.de
authors.forename: Stanislao
authors.initials: S
authors.lastname: Morgera
authors.forename: Michael
authors.initials: M
authors.lastname: Haase
authors.forename: Jens
authors.initials: J
authors.lastname: Rocktäschel
authors.forename: Torsten
authors.initials: T
authors.lastname: Böhler
authors.forename: Ortrud
authors.initials: O
authors.lastname: Vargas-Hein
authors.forename: Christoph
authors.initials: C
authors.lastname: Melzer
authors.forename: Dietmar
authors.initials: D
authors.lastname: Krausch
authors.forename: Wolfgang J
authors.initials: WJ
authors.lastname: Kox
authors.forename: Gerd
authors.initials: G
authors.lastname: Baumann
authors.forename: Werner
authors.initials: W
authors.lastname: Beck
authors.forename: Hermann
authors.initials: H
authors.lastname: Göhl
authors.forename: Hans-H
authors.initials: HH
authors.lastname: Neumayer
mesh_terms: D058186:Acute Kidney Injury / Q000097:blood / Q000503:physiopathology / Q000628:therapy; D002199:Capillary Permeability; D005260:Female; D006440:Hemofiltration / Q000379:methods*; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D007963:Leukocytes, Mononuclear / Q000378:metabolism / Q000502:physiology; D008297:Male; D009102:Multiple Organ Failure / Q000097:blood / Q000503:physiopathology / Q000628:therapy*; D009504:Neutrophils / Q000378:metabolism / Q000502:physiology; D010587:Phagocytosis / Q000502:physiology; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood / Q000503:physiopathology / Q000628:therapy*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D018836:Inflammation Mediators; D014409:Tumor Necrosis Factor-alpha