title: Lung-protective mechanical ventilation does not protect against acute kidney injury in patients without lung injury at onset of mechanical ventilation.
abstract: BACKGROUND
  Preclinical and clinical studies suggest that mechanical ventilation contributes to the development of acute kidney injury (AKI), particularly in the setting of lung-injurious ventilator strategies.
  
  
  OBJECTIVE
  To determine whether ventilator settings in critically ill patients without acute lung injury (ALI) at onset of mechanical ventilation affect the development of AKI.
  
  
  METHODS
  Secondary analysis of a randomized controlled trial (N = 150), comparing conventional tidal volume (V(T), 10 mL/kg) with low tidal volume (V(T), 6 mL/kg) mechanical ventilation in critically ill patients without ALI at randomization. During the first 5 days of mechanical ventilation, the RIFLE class was determined daily, whereas neutrophil gelatinase-associated lipocalin and cystatin C levels were measured in plasma collected on days 0, 2, and 4.
  
  
  RESULTS
  Eighty-six patients had no AKI at inclusion, and 18 patients (21%) subsequently developed AKI, but without significant difference between ventilation strategies. (Cumulative hazard, 0.26 vs 0.23; P = .88.) The courses of neutrophil gelatinase-associated lipocalin and cystatin C plasma levels did not differ significantly between randomization groups.
  
  
  CONCLUSIONS
  In the present study in critically patients without ALI at onset of mechanical ventilation, lower tidal volume ventilation did not reduce the development or worsening of AKI compared with conventional tidal volume ventilation.
authors.affiliation: Laboratory of Experimental Intensive Care and Anesthesiology (LEICA), Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. bartcortjens@hotmail.com
authors.forename: Bart
authors.initials: B
authors.lastname: Cortjens
authors.forename: Annick A N M
authors.initials: AA
authors.lastname: Royakkers
authors.forename: Rogier M
authors.initials: RM
authors.lastname: Determann
authors.forename: Jeroen D E
authors.initials: JD
authors.lastname: van Suijlen
authors.forename: Stephan S
authors.initials: SS
authors.lastname: Kamphuis
authors.forename: Jannetje
authors.initials: J
authors.lastname: Foppen
authors.forename: Anita
authors.initials: A
authors.lastname: de Boer
authors.forename: Cathrien W
authors.initials: CW
authors.lastname: Wieland
authors.forename: Peter E
authors.initials: PE
authors.lastname: Spronk
authors.forename: Marcus J
authors.initials: MJ
authors.lastname: Schultz
authors.forename: Catherine S C
authors.initials: CS
authors.lastname: Bouman
mesh_terms: D000209:Acute-Phase Proteins; D055316:Cystatin C / Q000097:blood; D005260:Female; D006801:Humans; D000071068:Lipocalin-2; D054834:Lipocalins / Q000097:blood; D008297:Male; D008875:Middle Aged; D011518:Proto-Oncogene Proteins / Q000097:blood; D016032:Randomized Controlled Trials as Topic; D012121:Respiration, Artificial / Q000009:adverse effects / Q000379:methods*; D013990:Tidal Volume; D055397:Ventilator-Induced Lung Injury / Q000517:prevention & control*
chemical_list: D000209:Acute-Phase Proteins; D055316:Cystatin C; C489506:LCN2 protein, human; D000071068:Lipocalin-2; D054834:Lipocalins; D011518:Proto-Oncogene Proteins