More vasopressor, lower pressure: the refractory phenotype in cardiac-surgery AKI

Cardiac-surgery-associated acute kidney injury (CSA-AKI) is common and irreversible. Heavier early vasopressor use is linked to it; whether risk reflects achieved pressure or delivered dose is unclear. We describe these associations in two cohorts.

Two cohorts were analysed separately (not pooled): primary (n=9,969, 705 CSA-AKI, 7.1%) and replication (n=3,292, 190, 5.8%). Exposure was cumulative first-24h vasopressor dose-load (norepinephrine-equivalent); achieved mean arterial pressure (MAP) is post-treatment. Outcome was creatinine/renal replacement therapy (RRT)-defined KDIGO stage 2-3 within 7 days, death competing.

More vasopressor accompanied lower achieved MAP (rho -0.20 and -0.59). Higher dose-load was associated with CSA-AKI (adjusted OR per SD 1.25 [95% CI 1.16-1.35] and 2.96 [2.23-3.92]), persisting with exposure and outcome windows separated (landmark 1.22 and 3.29). Risk rose as achieved MAP fell (adjusted OR per SD 0.89 and 0.55). The highest-dose, lowest-pressure group - a descriptive high-risk haemodynamic phenotype ("refractory") - carried the greatest adjusted absolute excess (6.1% [3.0-9.6] and 9.9% [3.2-17.8]). Dose-load also predicted 28-day mortality, a non-renal outcome (OR 1.47 and 2.48), supporting its interpretation primarily as a marker of illness severity rather than evidence of direct kidney toxicity.

More vasopressor was not accompanied by higher achieved pressure; the patient whose dose climbs while pressure falls signals high kidney risk. These descriptive findings support recognising and monitoring this phenotype and enriching prospective trials; they establish no blood-pressure target (including 65 mmHg) and no case for dose reduction.