• Kathleen D Liu, David V Glidden, Mark D Eisner, Polly E Parsons, Lorraine B Ware, Arthur Wheeler, Anna Korpak, B Taylor Thompson, Glenn M Chertow, Michael A Matthay, and National Heart, Lung, and Blood Institute ARDS Network Clinical Trials Group.
• Division of Nephrology, University of California, San Francisco, CA, USA. Kathleen.liu@ucsf.edu
• Crit. Care Med. 2007 Dec 1;35(12):2755-61.

ObjectiveTo identify biological and clinical predictors of acute kidney injury in subjects with acute lung injury.DesignSecondary data analysis from a multicenter, randomized clinical trial.SettingIntensive care units in ten university medical centers.PatientsA total of 876 patients enrolled in the first National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome Clinical Network trial.InterventionsStudy subjects were randomized to receive a low tidal volume ventilation strategy and pharmacologic therapy with ketoconazole or lisofylline in a factorial design.Measurements And Main ResultsWe tested the association of baseline levels of interleukin-6, interleukin-8, interleukin-10, von Willebrand factor, tumor necrosis factor-[alpha], type I and II soluble tumor necrosis factor receptors (sTNFR-I and -II), protein C, plasminogen activator inhibitor-1 (PAI-1), surfactant protein-A, surfactant protein-D, and intracellular adhesion molecule-1 with subsequent acute kidney injury. Of 876 study participants who did not have end-stage renal disease, 209 (24%) developed acute kidney injury, defined as a rise in serum creatinine of >50% from baseline over the first four study days. The 180-day mortality rate for subjects with acute kidney injury was 58%, compared with 28% in those without acute kidney injury (p < .001). Interleukin-6, sTNFR-I, sTNFR-II, and PAI-1 levels were independently associated with acute kidney injury after adjustment for demographics, interventions, and severity of illness. A combination of clinical and biological predictors had the best area under the receiver operating characteristic curve, and the contribution of sTNFR-I and PAI-1 to this model was highly significant (p = .0003).ConclusionsElevations in PAI-1, interleukin-6, and the sTNFRs in subjects with acute kidney injury suggest that disordered coagulation, inflammation, and neutrophil-endothelial interactions play important roles in the pathogenesis of acute kidney injury. The combination of these biological and clinical risk factors may have important and additive value in predictive models for acute kidney injury.

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