Authors: Arora P et al.
Anesthesiology. November 21, 2025. DOI: 10.1097/ALN.0000000000005861
Summary
This double-blind, placebo-controlled randomized clinical trial evaluated whether inhaled nitric oxide (NO) can reduce postoperative acute kidney injury (AKI) in high-risk cardiac surgery patients with pre-existing endothelial dysfunction. Endothelial dysfunction is marked by impaired endogenous nitric oxide synthesis, and prolonged cardiopulmonary bypass (CPB) increases hemolysis and further reduces NO bioavailability—making this population a plausible target for NO therapy.
A total of 250 adults undergoing cardiac surgery with CPB lasting longer than 90 minutes were randomized to receive either 80 ppm NO (during bypass and for 24 hours postoperatively) or an identical placebo gas mixture. The primary endpoint was AKI by KDIGO criteria; secondary endpoints included AKI staging and need for renal replacement therapy (RRT) during hospitalization and up to one year.
AKI occurred in 44.0% of patients in the NO group and 43.2% in the placebo group, yielding an adjusted odds ratio of 1.00 (95% CI 0.59–1.69). None of the secondary outcomes—including severity of AKI, in-hospital RRT, or RRT required at 6 weeks, 90 days, or one year—differed meaningfully between groups. The findings therefore do not support any measurable kidney-protective effect of NO in this specific population.
Key Points
• In 250 cardiac surgery patients with endothelial dysfunction, inhaled NO at 80 ppm did not reduce AKI.
• Rates of AKI were nearly identical between NO and placebo groups.
• No improvement was seen in AKI severity or need for renal replacement therapy at any follow-up point.
• This trial does not support routine perioperative NO therapy for AKI prevention in patients with endothelial dysfunction undergoing prolonged CPB.
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