Two separately analysed cardiac-surgery cohorts included 9,969 and 3,292 patients, with CSA-AKI occurring in 7.1% and 5.8%, respectively. The endpoint was creatinine/RRT-defined KDIGO stage 2–3 AKI within seven days, with death treated as a competing event. Higher first-24-hour vasopressor dose-load was associated with AKI: adjusted odds ratios per standard deviation were 1.25 (95% CI 1.16–1.35) and 2.96 (2.23–3.92). Greater vasopressor exposure accompanied lower achieved mean arterial pressure in both cohorts, and the highest-dose, lowest-pressure phenotype had the greatest adjusted absolute excess kidney risk.
Escalating vasopressor exposure alongside low achieved pressure identified a high-risk postoperative phenotype. These associations do not establish vasopressor kidney toxicity, a blood-pressure target, or benefit from dose reduction.
Study limitation: Achieved pressure was measured after treatment, and illness severity may explain the associations rather than a causal effect of vasopressors.
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