17 research outputs found

    Serum Cystatin C as an Early Marker of Neutrophil Gelatinase‐associated Lipocalin‐positive Acute Kidney Injury Resulting from Cardiopulmonary Bypass in Infants with Congenital Heart Disease

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    ObjectiveAcute kidney injury (AKI) is a common complication resulting from cardiopulmonary bypass in infants. Urinary neutrophil gelatinase‐associated lipocalin (NGAL) is a sensitive and specific marker of such injury. In this study, we compared the performance of serum cystatin C (Cys C) and serum creatinine (Cr) as early markers of renal dysfunction in infants undergoing cardiac surgery under bypass.Study Design, Setting, and PatientsThe study was designed as a prospective observational study. The study was conducted in the cardiac intensive care unit (ICU) of a tertiary, academic children's hospital in the United States. Infants (age <1 year) undergoing cardiac surgery under cardiopulmonary bypass were included in the study.Outcome MeasureAcute kidney injury was defined based on postoperative urinary NGAL.ResultsA total of 17 infants were included in the study, and five of them developed AKI. Serum Cys C and Cr levels were measured postoperatively on days 1, 2, and 3, and compared with baseline levels. On postoperative day 2, infants with AKI showed significant change from baseline in serum Cys C levels compared with non‐AKI infants (28% vs. −9%, P = .03). The two groups did not show significant differences with respect to rise in serum Cr on any of the 3 postoperative days. Serum Cr on days 1 and 2 showed nonspecific increases in both AKI and non‐AKI groups. The area under the receiver operating characteristic curve for day 2 Cys C was 0.87 (95% CI 0.67–1.00) in recognizing NGAL‐positive AKI.ConclusionsPostoperative serum Cys C appears to be a more specific and sensitive biomarker for NGAL‐positive AKI resulting from cardiopulmonary bypass surgery in infants undergoing cardiac surgery.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/113151/1/chd12253.pd

    Mechanisms employed by retroviruses to exploit host factors for translational control of a complicated proteome

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