Abstract
CSA-AKI is common after cardiac surgery, and even small increases in serum creatinine are associated with significant increases morbidity and mortality. A variety of risk factors have been identified for the development of CSA-AKI, but a precise precipitating event or events which lead to this complication have yet to be identified. Moreover, current diagnostic methods for detecting AKI lag behind the point of injury by 24-48 hours. Current technologies to close this gap include biomarkers and cerebral autoregulation monitoring data, but clear methodologies for their use have yet to be perfected. There have similarly been many failed interventions aimed at ameliorating AKI, though goal-directed perfusion strategies on CPB may hold promise.
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