title: On-line hemodiafiltration does not induce inflammatory response in end-stage renal disease patients: results from a multicenter cross-over study.
abstract: BACKGROUND
  On-line hemodiafiltration (HDF) represents the supreme blood purification modality for end-stage renal disease (ESRD) patients. Large-volume infusion of on-line prepared substitution fluid may, however, expose patients to inflammatory contaminants. As a result, on-line HDF might aggravate chronic inflammation, which correlates with malnutrition, cardiovascular disease, and mortality among ESRD patients.
  
  
  METHODS
  In a multicenter cross-over study, 27 ESRD patients were randomly assigned to treatment with on-line HDF and low-flux hemodialysis (HD). After 6 months, patients were crossed to the other treatment modality, and treatment continued for another 6 months. Both on-line HDF and low-flux HD were conducted with polysulfone membranes and ultrapure dialysis fluid. Samples were drawn at the end of each treatment period.
  
  
  RESULTS
  Inflammatory parameters were elevated in the study population when compared to healthy controls. Induction of interleukin-1 receptor antagonist (IL-1Ra) and tumor necrosis factor alpha (TNF-alpha) was comparable for on-line HDF and low-flux HD, and there was no intradialytic increase in cytokine production. As a result, interleukin-6 (IL-6) plasma levels did not differ significantly between the two treatment modalities. Similarly, no difference between on-line HDF and low-flux HD was observed for C-reactive protein (CRP) and albumin. Markers of endothelial cell activation (soluble intercellular and vascular cell adhesion molecules sICAM-1 and sVCAM-1) as well as the cardiovascular risk marker cardiac troponin T (cTnT) remained elevated compared to healthy subjects, but showed no difference between the two treatment modalities.
  
  
  CONCLUSIONS
  On-line HDF, as the most effective renal replacement therapy, does not provoke inflammatory response and is both safe and highly biocompatible.
authors.affiliation: 2nd Medical School, University of Debrecen, Debrecen, Hungary.
authors.forename: Lajos R
authors.initials: LR
authors.lastname: Vaslaki
authors.forename: Klara
authors.initials: K
authors.lastname: Berta
authors.forename: Lajos
authors.initials: L
authors.lastname: Major
authors.forename: Viktoria
authors.initials: V
authors.lastname: Weber
authors.forename: Christoph
authors.initials: C
authors.lastname: Weber
authors.forename: Ralf
authors.initials: R
authors.lastname: Wojke
authors.forename: Jutta
authors.initials: J
authors.lastname: Passlick-Deetjen
authors.forename: Dieter
authors.initials: D
authors.lastname: Falkenhagen
mesh_terms: D000328:Adult; D000368:Aged; D000418:Albumins / Q000032:analysis; D002097:C-Reactive Protein / Q000032:analysis; D018592:Cross-Over Studies; D016207:Cytokines / Q000097:blood; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D017583:Hemodiafiltration / Q000009:adverse effects / Q000379:methods*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D007375:Interleukin-1 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D007676:Kidney Failure, Chronic / Q000097:blood / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D016896:Treatment Outcome; D020107:Troponin T / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D000418:Albumins; D016207:Cytokines; D007375:Interleukin-1; D015850:Interleukin-6; D020107:Troponin T; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein