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Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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In trauma ICU patients, acute kidney injury (AKI) reflects systemic hypoperfusion, tubular dysfunction, and microcirculatory imbalance. Conventional biomarkers detect damage late, whereas physiologic indices may reveal earlier, and potentially reversible renal stress. We evaluated urinary sodium (NaU) and the fractional excretion of potassium (FEK), introducing a Microcirculatory Stress Index (MSI = NaU/FEK) to capture microcirculatory–tubular stress.
We conducted a prospective observational cohort of 168 adult trauma ICU patients (May 2024–October 2025). AKI, defined by KDIGO, was assessed daily during ICU hospitalization. From admission, serial NaU, urine potassium, and urine creatinine were obtained alongside routine laboratory and clinical variables. AKI predictors were NaU, FEK, mean arterial pressure (MAP), and lactate. Logistic regression and ROC analyses evaluated the prediction of AKI onset and of recovery; MSI quantified microcirculatory stress.
AKI occurred in 54.2% of patients (Stage I 22.0%, Stage II 13.7%, Stage III 18.5%). Notably, 23% of AKI cases emerged by ICU day 2, indicating injury typically within 48 hours of admission. For early AKI prediction, NaU <46 mmol/L yielded an AUC of 0.635, a specificity of 87%, and a sensitivity of 46%, identifying low NaU as a particular early warning signal. Adding FEK improved discrimination: the combined rule NaU < 44.4 mmol/L or FEK ≥ 42.4 achieved a sensitivity of 59%, a specificity of 81%, and the highest Youden’s index (0.399), with an AUC ≈ of approximately 0.70 compared to approximately 0.635 for NaU alone [Figure 1]. MSI <1.0 provided an AUC of 0.70, with sensitivity at 59% and specificity at 81%, offering greater sensitivity while holding reasonable specificity. A model incorporating MAP <70 mmHg, lactate ≥2.3 mmol/L, and NaU had an AUC of 0.64. For recovery prediction, NaU ≥60 mmol/L generated an AUC of 0.68, a sensitivity of 80%, and a specificity of 65%; notably, NaU exceeded 60 mmol/L approximately 24–48 hours before clinical resolution and was found consistent with the restoration of tubular flow and microcirculatory perfusion [Figure 2].
Conclusion: Low NaU and MSI <1.0, signal early microcirculatory stress and predict AKI onset, whereas rising NaU ≥60 mmol/L foresees recovery. Integrating NaU, FEK, MAP, and lactate provides a pragmatic, bedside framework for real-time renal risk assessment and recovery monitoring in trauma ICU patients.
Clinical Implications: MSI (NaU/FEK) is an inexpensive, rapidly obtainable index that enhances early AKI detection and helps time escalation or de-escalation of therapies, supporting personalized resuscitation and stewardship of potentially nephrotoxic exposures.
Funding: This research is part of the project funded by the National Agency for Scientific Research and Innovation (NASRI).
