• Catherine D Krawczeski, Rene G Vandevoorde, Thelma Kathman, Michael R Bennett, Jessica G Woo, Yu Wang, Rachel E Griffiths, and Prasad Devarajan.
• The Heart Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229-3039, USA. catherine.krawczeski@cchmc.org
• Clin J Am Soc Nephrol. 2010 Sep 1;5(9):1552-7.

Background And ObjectivesAcute kidney injury (AKI) is a frequent complication of cardiopulmonary bypass (CPB). Serum creatinine (SCr), the current standard, is an inadequate marker for AKI since a delay occurs before SCr rises. Biomarkers that are sensitive and rapidly measurable could allow early intervention and improve patient outcomes. We investigated the value of serum cystatin C as an early biomarker for AKI after pediatric CPB.Design, Setting, Participants, & MeasurementsWe analyzed data from 374 prospectively enrolled children undergoing CPB. Serum samples were obtained before and at 2, 12, and 24 hours after CPB. Cystatin C was quantified by nephelometry. The primary outcome was AKI, defined as a > or =50% increase in SCr. Secondary outcomes included severity and duration of AKI, hospital length of stay, and mortality. A multivariable stepwise logistic regression analysis was used to assess predictors of AKI.ResultsOne hundred nineteen patients (32%) developed AKI using SCr criteria. Serum cystatin C concentrations were significantly increased in AKI patients at 12 hours after CPB (P < 0.0001) and remained elevated at 24 hours (P < 0.0001). Maximal sensitivity and specificity for prediction of AKI occurred at a 12-hour cystatin C cut-off of 1.16 mg/L. The 12-hour cystatin C strongly correlated with severity and duration of AKI as well as length of hospital stay. In multivariable analysis, 12-hour cystatin C remained a powerful independent predictor of AKI.ConclusionSerum cystatin C is an early predictive biomarker for AKI and its clinical outcomes after pediatric CPB.

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