Mitochondrial oxygenation monitoring and acute kidney injury risk in cardiac surgery: A prospective cohort study

Cardiac surgery-associated acute kidney injury (CSA-AKI) is a common complication of cardiac surgery and is associated with increased morbidity and mortality. Recent guidelines emphasize the need for new monitoring methods to facilitate targeted CSA-AKI prevention and treatment strategies. In vivo real-time measurement of mitochondrial oxygen tension (mitoPO 2 ), could potentially fulfil this role during cardiac surgery, as suggested in our previous pilot study. In this prospective observational study, we investigated 75 cardiac surgery patients with an increased preoperative CSA-AKI risk. The primary aim of this study was to assess whether patients who developed CSA-AKI experienced prolonged periods of mitoPO 2 < 20 mmHg during surgery. mitoPO 2 was measured intraoperatively, and CSA-AKI was defined according to the Kidney Disease: Improving Global Outcomes criteria. Four additional mitoPO 2 thresholds (<25, <30, <35, and < 40 mmHg) were analyzed, including the predictive capacity of all thresholds for CSA-AKI. This study found that patients who developed CSA-AKI had a significantly longer intraoperative time with mitoPO 2 <20 mmHg and <25, <30, <35, and <40 mmHg. Subsequently, we tested all thresholds for their association with the risk of CSA-AKI, with the <25 mmHg threshold demonstrating the highest significant odds ratio. Every minute spent below <25 mmHg increased the risk of CSA-AKI by 0.7 % ( P = 0.021). This study highlighted the association between mitoPO 2 and the onset of CSA-AKI. Extended durations below the mitoPO 2 threshold of 25 mmHg significantly correlate with an elevated CSA-AKI risk. Using mitoPO 2 as a monitoring tool shows promise in potentially predicting and possibly preventing CSA-AKI when used as a treatment trigger in cardiac surgery patients. • The CSA-AKI cohort exhibited significantly prolonged mitoPO 2 levels <20 mmHg. • Prolonged intraoperative mitoPO 2 <25 mmHg significantly increases CSA-AKI risk. • This study supports mitoPO 2 as a potential tool for targeted CSA-AKI prevention.