title: Acute kidney injury is associated with early cytokine changes after trauma.
abstract: BACKGROUND
  Acute kidney injury (AKI) occurs in 26% of trauma patients and is associated with increased mortality and risk for nosocomial infections (NCIs). We compared serial plasma cytokine levels in patients with posttraumatic AKI to determine whether the early cytokine changes are associated with the occurrence of AKI and NCI.
  
  
  METHODS
  We performed a secondary analysis of the Inflammation and the Host Response to Injury database to include adult blunt trauma patients who had available plasma proteomic analyses. AKI was defined by the RIFLE (Risk, Injury, Failure, Loss, and End-stage Kidney) classification, which requires a 50% increase in serum creatinine. The association among AKI, NCI, and plasma cytokines was analyzed using a mixed model analyses and logistic regression.
  
  
  RESULTS
  Among 147 patients in the cohort, prevalence of NCI was 73% and 52% for patients with and without AKI, respectively. In mixed model analyses adjusted for clinical factors, AKI patients developed significant early increase in IL-1ra, IL-8, MCP1, and IL-6; early decrease in sTNFR2; and late decrease in IL-1ra, IL-4, and IL-6 concentrations, compared with patients without AKI and regardless of NCI. The change in cytokine pattern differed for sIL1R2, CXCL1, and MIP1β, depending on the occurrence of NCI. Patients with AKI and NCI had lower early and late sIL1R2 and higher early and late CXCL1 and MIP1β levels. Within the first 24 hours of injury, adding plasma levels of IL-1ra, IL-8, MCP1, IL-6, and sTNFR2 to clinical parameters of injury severity provided a predictive model for AKI superior to clinical model only (p < 0.001).
  
  
  CONCLUSIONS
  AKI trauma patients exhibit simultaneous changes in proinflammatory and anti-inflammatory serial plasma cytokine levels. The predictive model for AKI that combines plasma cytokine levels with clinical data within 24 hours of injury requires further prospective validation in larger studies.
  
  
  METHODS
  Prognostic study, level III.
authors.affiliation: Division of Critical Care Medicine, University of Florida, Gainesville, FL 32610-0254, USA. abihorac@anest.ufl.edu
authors.forename: Azra
authors.initials: A
authors.lastname: Bihorac
authors.forename: Tezcan Ozrazgat
authors.initials: TO
authors.lastname: Baslanti
authors.forename: Alex G
authors.initials: AG
authors.lastname: Cuenca
authors.forename: Charles E
authors.initials: CE
authors.lastname: Hobson
authors.forename: Darwin
authors.initials: D
authors.lastname: Ang
authors.forename: Philip A
authors.initials: PA
authors.lastname: Efron
authors.forename: Ronald V
authors.initials: RV
authors.lastname: Maier
authors.forename: Frederick A
authors.initials: FA
authors.lastname: Moore
authors.forename: Lyle L
authors.initials: LL
authors.lastname: Moldawer
mesh_terms: D058186:Acute Kidney Injury / Q000097:blood* / Q000209:etiology; D000328:Adult; D002056:Burns / Q000097:blood / Q000150:complications*; D003428:Cross Infection / Q000097:blood / Q000453:epidemiology* / Q000209:etiology; D016207:Cytokines / Q000097:blood*; D005260:Female; D005431:Florida / Q000453:epidemiology; D006801:Humans; D015994:Incidence; D007249:Inflammation / Q000097:blood*; D008297:Male; D011379:Prognosis; D011446:Prospective Studies; D040901:Proteomics / Q000379:methods
chemical_list: D016207:Cytokines