TY - JOUR
T1 - Mitochondrial oxygenation monitoring and acute kidney injury risk in cardiac surgery
T2 - A prospective cohort study
AU - de Wijs, Calvin J.
AU - Streng, Lucia W.J.M.
AU - Stolker, Robert Jan
AU - ter Horst, Maarten
AU - Hoorn, Ewout J.
AU - Mahtab, Edris A.F.
AU - Mik, Egbert G.
AU - Harms, Floor A.
N1 - Publisher Copyright: © 2024 The Authors
PY - 2025/4
Y1 - 2025/4
N2 - Background: 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 (mitoPO2), could potentially fulfil this role during cardiac surgery, as suggested in our previous pilot study. Methods: 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 mitoPO2 < 20 mmHg during surgery. mitoPO2 was measured intraoperatively, and CSA-AKI was defined according to the Kidney Disease: Improving Global Outcomes criteria. Four additional mitoPO2 thresholds (<25, <30, <35, and < 40 mmHg) were analyzed, including the predictive capacity of all thresholds for CSA-AKI. Results: This study found that patients who developed CSA-AKI had a significantly longer intraoperative time with mitoPO2 <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). Conclusions: This study highlighted the association between mitoPO2 and the onset of CSA-AKI. Extended durations below the mitoPO2 threshold of 25 mmHg significantly correlate with an elevated CSA-AKI risk. Using mitoPO2 as a monitoring tool shows promise in potentially predicting and possibly preventing CSA-AKI when used as a treatment trigger in cardiac surgery patients.
AB - Background: 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 (mitoPO2), could potentially fulfil this role during cardiac surgery, as suggested in our previous pilot study. Methods: 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 mitoPO2 < 20 mmHg during surgery. mitoPO2 was measured intraoperatively, and CSA-AKI was defined according to the Kidney Disease: Improving Global Outcomes criteria. Four additional mitoPO2 thresholds (<25, <30, <35, and < 40 mmHg) were analyzed, including the predictive capacity of all thresholds for CSA-AKI. Results: This study found that patients who developed CSA-AKI had a significantly longer intraoperative time with mitoPO2 <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). Conclusions: This study highlighted the association between mitoPO2 and the onset of CSA-AKI. Extended durations below the mitoPO2 threshold of 25 mmHg significantly correlate with an elevated CSA-AKI risk. Using mitoPO2 as a monitoring tool shows promise in potentially predicting and possibly preventing CSA-AKI when used as a treatment trigger in cardiac surgery patients.
UR - http://www.scopus.com/inward/record.url?scp=85211082257&partnerID=8YFLogxK
U2 - 10.1016/j.jclinane.2024.111715
DO - 10.1016/j.jclinane.2024.111715
M3 - Article
C2 - 39657393
AN - SCOPUS:85211082257
SN - 0952-8180
VL - 101
JO - Journal of Clinical Anesthesia
JF - Journal of Clinical Anesthesia
M1 - 111715
ER -