Serum Cystatin C Is an Early Predictive Biomarker of Acute Kidney Injury after Pediatric Cardiopulmonary Bypass
ABSTRACT Acute 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.
We 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.
One 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.
Serum cystatin C is an early predictive biomarker for AKI and its clinical outcomes after pediatric CPB.
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ABSTRACT: While emerging evidence indicates that the incidence of both acute kidney injury (AKI) and chronic kidney disease (CKD) in children is rising and that the etiologies are dramatically changing, relatively little is currently known regarding the potential for transition from AKI to CKD. Major barriers to assessing for a potential AKI to CKD link have included lack of a standard pediatric AKI definition, narrow focus only on children with AKI who receive renal replacement therapy, and reliance on serum creatinine as the main biomarker to detect and diagnose AKI and CKD. Recent data have validated a multi-dimensional AKI classification system for children and have suggested chronic kidney sequelae in pediatric populations with AKI or at risk for AKI. In addition, a number of novel AKI biomarkers are being rigorously validated as early indicators of incipient CKD. Our goals for this article are to (1) review the recent changes in pediatric AKI and CKD epidemiology, (2) explore the evidence for a potential AKI to CKD link, and (3) propose new clinical and research paradigms to better elucidate the progression from AKI to CKD.Pediatric Nephrology 10/2010; 26(4):509-22. DOI:10.1007/s00467-010-1653-4
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