Acute kidney injury (AKI) remains one of the most frequent complications after cardiac surgery and is associated with nearly 40% mortality at 5 years (1). These concerning outcomes have led many authors to focus on the prevention, early detection, and treatment of cardiac surgery-associated AKI (CSA-AKI), with limited success so far. According to Kidney Disease Improving Global Outcome (KDIGO) criteria, AKI is defined by an increase in serum creatinine and/or a decrease in urine output (2). However, this functional definition does not reflect the different stages of kidney injury, ranging from renal hypoperfusion without structural damage (“pre-renal azotemia”), to structural injury without loss of function (“subclinical AKI”), and finally intrinsic AKI with both damage and functional impairment, which is the stage clinicians aim to prevent (3).

An intuitive approach to avoid abnormal renal perfusion and to prevent AKI is to maintain or increase systemic oxygen delivery (DO₂) by applying the concept of goal-directed perfusion (4,5). It is from this perspective that Wijk et al., a Swedish research team with expertise in CSA-AKI and renal oxygenation, performed a randomized controlled trial called “Effects of Increased Cardiopulmonary Bypass Pump Flow on Renal Filtration, Perfusion, Oxygenation, and Tubular Injury in Cardiac Surgical Patients: A Randomized Controlled Trial” and published in Anesthesiology in October 2025 (6). The authors presented a physiological comparison of standard flow (SF; 2.4 L/min/m²) versus high flow (HF; 2.9 L/min/m²) cardiopulmonary bypass (CPB) pump flow, assessing renal blood flow (RBF), filtration, oxygenation, and tubular injury in 36 randomized patients undergoing on-pump cardiac surgery.

The originality and strength of this study lie in its integrated and multimodal physiological approach, which combines direct measurements of renal hemodynamics and function to provide an unusually detailed in vivo characterization of the human kidney during CPB. Despite a clear increase in systemic blood flow and systemic DO₂ with HF CPB, RBF remained unchanged, and renal oxygen delivery (RDO₂) paradoxically decreased in SF and HF groups. In contrast, renal function improved in HF group compared to SF group: glomerular filtration rate (GFR) and sodium filtration increased while tubular sodium reabsorption showed a non-significant trend toward increase (see Table 1). Additionally, urinary N-acetyl-β-D-glucosaminidase (NAG), marker of tubular injury, increased only in the SF group.