- Design
- Retrospective single-centre cohort with entropy balancing
- Population
- 30,039 adults after non-cardiac surgery in South Korea
- Primary outcome
- Postoperative acute kidney injury
- Effect
- Narrow pulse pressure OR 1.66 (1.42 to 1.94); with normotension OR 1.56 (1.27 to 1.89)
This single-centre South Korean cohort analysed 30,039 adults having non-cardiac surgery between 2011 and 2020, grouped by median intraoperative pulse pressure and adjusted for vasopressor load and hypotension duration.
AKI occurred in 6.7%. Narrow pulse pressure (below 40 mmHg) was associated with AKI compared with 40 to 70 mmHg (OR 1.66, 95% CI 1.42 to 1.94). Normotension with narrow pulse pressure was associated with AKI (OR 1.56), whereas hypotension with normal pulse pressure was not (OR 1.09, 0.86 to 1.38). The combination carried the highest risk (OR 1.85). Stroke volume index was much lower in the normotensive narrow pulse pressure group (27 vs 47 mL/m²). Risk became significant after 40 minutes of exposure.
The finding challenges an exclusively MAP-based target: a normal MAP produced by vasoconstriction over a low stroke volume may still underperfuse the kidney. It is observational and cannot show that correcting pulse pressure prevents AKI, but it is a cheap signal already on the monitor.
- Watch pulse pressure as well as MAP; a sustained value below 40 mmHg may signal low stroke volume.
- Consider fluid responsiveness or cardiac output assessment rather than more vasopressor when MAP is normal but pulse pressure is narrow.
- Pay particular attention when narrow pulse pressure lasts more than about 40 minutes.
- Record pulse pressure trends in the anaesthetic chart for patients at AKI risk.
Why it matters
It questions whether a MAP target alone protects the kidneys.
Don't overread it
Retrospective and single-centre; it shows association, not that treating pulse pressure prevents AKI.
The statistics, in plain English
An odds ratio of 1.56 means the odds of AKI were about 50% higher. Hypotension with normal pulse pressure had an interval crossing 1.0 (0.86 to 1.38), so it could not be separated from no effect in this cohort.
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