Abstract
Cardiac surgery–associated acute kidney injury (AKI) is linked to adverse outcomes including an increased risk of death, postoperative complications, and higher rates of incident or progressive chronic kidney disease.1,2 The cause of cardiac surgery–associated AKI is multifactorial. It is also well recognized that hemodynamic alterations can result in “functional” AKI, in which the glomerular filtration rate (GFR) decreases acutely without clinically significant tubular cell injury. In this latter context, the risk of adverse outcomes is lower. In 1983, the administration of a protein load was shown to increase GFR. This finding introduced the concept of renal functional reserve,3 which is .
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