Hilderink Bashar N, Crane Reinier F, Arbous Sesmu M, van den Bogaard Bas, Pillay Janesh, Juffermans Nicole P
Department of Intensive Care, OLVG Hospital, Amsterdam, the Netherlands; Laboratory of Translational Intensive Care, Erasmus MC, University Medical Center, Rotterdam, the Netherlands.
Department of Intensive Care, OLVG Hospital, Amsterdam, the Netherlands.
J Crit Care. 2025 Aug;88:155088. doi: 10.1016/j.jcrc.2025.155088. Epub 2025 Apr 22.
Dissociation between the micro- and macrocirculation as well as the lack of specificity of current markers to signal impaired tissue oxygenation complicate the timely diagnosis and treatment of tissue hypoperfusion to prevent acute kidney injury (AKI) after cardiac surgery. The newly developed non-invasive technique to measure the mitochondrial oxygenation (mitoPO2) is currently the most downstream bedside marker of tissue oxygenation. The aim was to investigate mitoPO2 as an early marker of postoperative development of AKI.
In a prospective observational study, postoperative mitochondrial oxygen tension was measured to detect AKI (defined by KDIGO) in patients undergoing cardiac surgery.
Of 50 included patients, 44 patients had analyzable mitoPO2 signal. 5 patients developed AKI. MitoPO2 at ICU admission was 16(13.8-24.6)mmHg in patients who developed AKI vs 63.4(37.5-77.9) mmHg in patients without AKI (p < 0.001). MitoPO2 predicted AKI (ROC 0.95 (0.89-1.0) with an optimal cut-off value of 30 mmHg (OR 4.4, CI 2.8-6.0, p < 0.001). Also, longer period of time under the mitoPO2 threshold predicted AKI with an AUROC of 0.91(0.80-1.00). In all patients, a decreased mitoPO2 occurred 4 h earlier than an clinically relevant increase in serum lactate. Other markers of tissue hypoperfusion, did not differ between patients with and without AKI.
A mitoPO2 value below 30 mmHg at ICU admission as well as the duration below this threshold indicate the development of AKI in cardiac surgery patients, occurring earlier than an increase in lactate above the normal range.
