![]() For AKI patients only we tested the additional effect of survival status as no deaths were observed in no AKI group. For each cytokine we modeled change over time of log-transformed cytokine concentration while accounting for time, AKI, nosocomial infections, and all two-way interactions. We utilized mixed model analysis of longitudinal changes in cytokines in order to properly account for correlations among repeated measurements for each patient. The analytical plan followed the STROBE recommendations for observational cohort studies 13 ( SDC, Methods). Time of measurements after injury was categorized as less than 12 hours (Day 0), 24-96 hours (Day 1-4) and ≥96 hours (≥Day 4). Cytokine concentrations from thawed plasma were assayed with the LINCOplex kit (Millipore, Billerica, MA) using the LUMINEX (Millipore) technology according to analytical protocols 12 ( SDC, Table 1). ![]() Duration of renal replacement therapy (RRT) was obtained from the database. RIFLE-R corresponds to a 50% increase in sCr, RIFLE-I to a two-fold increase in sCr, and RIFLE-F to a three-fold increase in sCr. Patients with RIFLE-AKI were stratified by severity determined by comparing the highest sCr with the RsCr. For the reference sCr we used the lower of two values: the lowest measured sCr in the first 24 hours after trauma or the estimated sCr as previously described 1. AKI was defined by the RIFLE classification using the change in sCr during the first 28 days of hospitalization compared to reference sCr (RsCr) 11. Nosocomial infections and clinical covariates were defined by the Glue Grant protocol 10 ( Supplemental Digital Content (SDC), Methods). The goal of this study was to assess the longitudinal change in serum cytokine levels among patients with severe blunt trauma enrolled in the Glue Grant database and their association with RIFLE-AKI and nosocomial infections. General liu rifle storm pro#Since animal models of ischemic AKI have implicated complex changes in both pro and anti-inflammatory cytokine profile in association with kidney injury 5, 6, 9 we hypothesized that trauma patients with AKI may exhibit a similar changes in cytokine profile over time and that an increased prevalence of NCI among AKI trauma patients may reflect this association. Previous studies of system-wide inflammation after trauma using quantification of serum cytokine levels from the TRDB demonstrated elevated levels of interleukin 6 (IL-6) and IL-10 as predictors of poor outcomes following trauma 8. The Trauma-Related DataBase (TRDB), a large multicenter database, contains prospectively collected clinical and biological data as a part of the Inflammation and the Host Response to Injury (Glue Grant), a large-scale interdisciplinary research program funded by the National Institute of General Medical Sciences to uncover the biological reasons for different clinical outcomes after traumatic injury. It is recognized that critically ill patients with severe AKI have an increased prevalence of infection 4, and we have recently demonstrated a higher prevalence of nosocomial infections (NCI) among trauma patients with even less severe stages of RIFLE-AKI 7. AKI is characterized by local and systemic inflammatory reaction where many locally produced cytokines mediate not only AKI itself, but also exert distant organ injury through systemic release from leukocytes in the kidneys and renal tubular cells 4- 6. ![]() RIFLE-AKI occurs in up to 26% of trauma patients and is associated with increased morbidity, mortality and cost 1, 2. The introduction of the RIFLE-AKI (Risk, Injury, Failure, Loss, and End-stage Kidney), a consensus definition for AKI, has increased awareness of the adverse effects of small changes in serum creatinine (sCr) level among different patient populations, and has facilitated a more uniform reporting of the prevalence and consequences of AKI 3. Although acute kidney injury (AKI) is independently associated with adverse outcomes among critically ill patients, only recently has it become appreciated as a common and serious complication of trauma 1, 2. ![]()
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