Association between Clinician-selected Mean Arterial Pressure Targets and Acute Kidney Injury in Patients with Septic Shock: A Prospective Cohort Study

Abstract

Background: Optimal mean arterial pressure (MAP) targets for preventing acute kidney injury (AKI) in patients with septic shock remain uncertain. This study compared the incidence of AKI between lower and higher MAP targets in patients with septic shock admitted to the intensive care unit (ICU) and explored factors associated with AKI.
Methods: This observational analytic comparative study used a prospective cohort design and was conducted in the ICU of Dr. Wahidin Sudirohusodo Hospital from May to July 2026. MAP targets were determined by the treating ICU team as part of routine clinical care, according to the hospital protocol. The investigators did not assign treatment targets. Patients were classified according to the prescribed MAP target (65–70 or 80–85 mmHg) at the 6-hour evaluation after initial resuscitation, provided that the target was achieved at that evaluation. Forty adult patients with septic shock were included and classified according to clinician-selected MAP targets of 65–70 mmHg (lower-target group, n=20) or 80–85 mmHg (higher-target group, n=20). The clinical and laboratory data, vasoactive-inotropic score (VIS), AKI incidence, and neutrophil gelatinase-associated lipocalin (NGAL) levels were assessed. Exploratory logistic regression analysis was performed to examine factors associated with AKI.
Results: AKI occurred in 4 patients (20.0%) in the low-MAP group and 7 patients (35.0%) in the high-MAP group; the difference was not statistically significant (Fisher's exact P=0.480). The risk difference was 15 percentage points (95% CI −12.3 to 42.3) and the risk ratio was 1.75 (95% CI 0.61–5.05), indicating an imprecise estimate. VIS was significantly higher in the high-MAP group throughout the observation period (p<0.001). NGAL levels were consistently higher among patients who developed AKI in both MAP groups. In exploratory logistic regression, ΔNGAL was associated with AKI (OR 1.08, 95% CI 1.03–1.14; p=0.003); the final model contained ΔNGAL alone.
Conclusions: In this small prospective cohort of patients with septic shock, no statistically significant difference in AKI occurrence was detected between the lower- and higher-MAP target groups. The estimate was imprecise, and the study was not designed to establish equivalence or causality. Higher MAP was accompanied by greater vasoactive-inotropic support. Changes in serum NGAL were associated with AKI in exploratory analyses and require validation in larger cohorts.