Extract

Following cardiac surgery with bypass, up to 40% of patients develop acute kidney injury (AKI), with 3%–10% developing severe AKI (KDIGO stage 2 or 3) [1, 2]. Cardiac surgery–associated AKI (CS-AKI) is associated with higher mortality, cardiovascular and infectious complications, an increased risk of de novo or progressive chronic kidney disease (CKD) and high healthcare costs. In the setting of cardiac surgery, in-hospital mortality in patients with no or stage 1 AKI is <5% but increases to 45% in patients with severe AKI requiring kidney replacement therapy (KRT). Preventing AKI may thus translate to better overall and kidney outcomes and reduced healthcare costs. For CS-AKI stage 1, associations with de novo CKD 1 year after cardiac surgery have been reported [3], but this may only hold true for patients with AKI that persists for >48 h [4]. The etiology of CS-AKI is multifactorial, including reduced kidney perfusion with secondary renal medullary hypoxia, tubular injury related to hemolysis, activation of coagulation and systemic inflammation [1]. Importantly, alterations in hemodynamics and volume status can result in “functional” AKI, where glomerular filtration rate (GFR) falls acutely without significant tubular cell injury [1]. In this setting, the risk of adverse outcomes is lower.

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