title: TNF-α depuration is a predictor of mortality in critically ill patients under continuous veno-venous hemodiafiltration treatment.
abstract: BACKGROUND
  Critically ill patients with acute kidney injury (AKI) present high mortality rates. The magnitude of inflammatory response could determine the prognosis of such patients. Continuous renal replacement therapy (CRRT) may play an important role in removing inflammatory mediators in patients with AKI.
  
  
  OBJECTIVE
  To investigate whether the magnitude of inflammatory mediator's removal is associated with mortality among critically ill patients on CVVHDF, a CRRT modality.
  
  
  METHODS
  This study consisted of 64 critically ill patients requiring CVVHDF. Plasma levels of C3a, TNF-α, IL-10, IL-6, IL-1β, sTNFRI and sTNFRII were determined by enzyme-linked immunosorbent assay (ELISA) at the beginning of CVVHDF and after 24h (outlet). Clearance of cytokines during the first 24h of CVVHDF was calculated. Clinical and laboratory data were acquired from patient's records data.
  
  
  RESULTS
  Mean age of patients requiring CVVHDF was 63years, 67.2% were men and 87.3% were Caucasian. Thirty-five (35) patients (54.7%) died. Comparing non-survivors with the group of survivors we observed higher incidence of sepsis (68.6 versus 37.9%, p<0.05), higher APACHE II score (34.8±7.6 versus 29.2±7.1, p<0.05) and higher lactate levels (23.2±17.6 versus 16.4±6.6, p<0.05). According to the inter-tertile range of TNF-α clearance (ITR1 (<0.54); ITR2 (0.54-2.93); ITR3 (>2.93)) we found that those patients with higher TNF-α removal by RRT (ITR3) had a better survival. Multivariable analysis showed that lower clearance of TNF-α remained independently associated with high mortality after adjustment for sex, age, use of vasoactive drugs, APACHE II score sepsis, creatinine and lactate before CVVHDF (HR: 0.179, 95% IC: 0.049-0.661, p<0.01).
  
  
  CONCLUSIONS
  The attenuation of inflammatory response may be related to the lower mortality observed on those patients with higher TNF-α removal by CVVHDF.
authors.affiliation: Universidade Federal de São Paulo, Department of Medicine, Nephrology Division, São Paulo, Brazil. Electronic address: marie@nefro.epm.br.
authors.forename: Beata Marie R
authors.initials: BM
authors.lastname: Quinto
authors.affiliation: Hospital Israelita Albert Einstein, São Paulo, Brazil.
authors.forename: Ilson J
authors.initials: IJ
authors.lastname: Iizuka
authors.affiliation: Hospital Israelita Albert Einstein, São Paulo, Brazil; Universidade Federal de São Paulo, Department of Medicine, Nephrology Division, São Paulo, Brazil.
authors.forename: Julio C M
authors.initials: JC
authors.lastname: Monte
authors.affiliation: Hospital Israelita Albert Einstein, São Paulo, Brazil.
authors.forename: Bento F
authors.initials: BF
authors.lastname: Santos
authors.affiliation: Hospital Israelita Albert Einstein, São Paulo, Brazil.
authors.forename: Virgílio
authors.initials: V
authors.lastname: Pereira
authors.affiliation: Hospital Israelita Albert Einstein, São Paulo, Brazil; Universidade Federal de São Paulo, Department of Medicine, Nephrology Division, São Paulo, Brazil.
authors.forename: Marcelino S
authors.initials: MS
authors.lastname: Durão
authors.affiliation: Hospital Israelita Albert Einstein, São Paulo, Brazil; Universidade Uninove, São Paulo, Brazil.
authors.forename: Maria A
authors.initials: MA
authors.lastname: Dalboni
authors.affiliation: Hospital Israelita Albert Einstein, São Paulo, Brazil; Universidade Federal de São Paulo, Department of Medicine, Nephrology Division, São Paulo, Brazil.
authors.forename: Miguel
authors.initials: M
authors.lastname: Cendoroglo
authors.affiliation: Hospital Israelita Albert Einstein, São Paulo, Brazil; Universidade Federal de São Paulo, Department of Medicine, Nephrology Division, São Paulo, Brazil.
authors.forename: Oscar F P
authors.initials: OF
authors.lastname: Santos
authors.affiliation: Hospital Israelita Albert Einstein, São Paulo, Brazil; Universidade Federal de São Paulo, Department of Medicine, Nephrology Division, São Paulo, Brazil; Tufts University School of Medicine, Nephrology Division, MA, USA.
authors.forename: Marcelo C
authors.initials: MC
authors.lastname: Batista
mesh_terms: D058186:Acute Kidney Injury / Q000401:mortality / Q000628:therapy*; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015926:Complement C3a / Q000378:metabolism; D016638:Critical Illness / Q000401:mortality / Q000628:therapy*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D017583:Hemodiafiltration / Q000379:methods*; D006801:Humans; D016753:Interleukin-10 / Q000097:blood; D053583:Interleukin-1beta / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000097:blood; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000097:blood; D015996:Survival Rate; D014409:Tumor Necrosis Factor-alpha / Q000097:blood* / Q000302:isolation & purification
chemical_list: D053583:Interleukin-1beta; D015850:Interleukin-6; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D015926:Complement C3a
keywords: AKI; CVVHDF; Critically ill patients; Cytokines; Inflammation