EARLY HEMODYNAMICS AND TREATMENT EXPOSURES PREDICT AKI, WHICH DRIVES MORTALITY AFTER TRAUMA ICU ADMISSION

In trauma intensive care, in-hospital acute kidney injury (AKI) and mortality remain high and are often preceded by early hemodynamic stress and cumulative therapeutic exposures. Recognizing bedside indicators of evolving organ dysfunction and imminent AKI within the first 24–48 hours can refine resuscitation priorities and guide prudent use of potentially harmful interventions.

We conducted a prospective observational cohort study at the University Hospital of Trauma, Albania (May 2024–October 2025). Adults admitted to the trauma ICU were followed for 14 days with standardized capture of demographics, illness severity, hemodynamics, diuresis/urine output, lactate, and early exposures (inotropes, NSAIDs, blood products). Sequential Organ Failure Assessment (SOFA) scores were intermittently (every 48–72 hours) recorded during the ICU stay; we analyzed peak SOFA and SOFA amplitude (max–min within 14 days). The primary outcome was in-hospital mortality. Multivariable logistic regression yielded adjusted odds ratios (aORs) with robust variance; ROC/AUC assessed discrimination.

Among 168 patients, AKI occurred in 54.2% (Stage I 22.0%, Stage II 13.7%, Stage III 18.5%). Most AKI developed early, by ICU Day 2 in 23% of those affected, indicating that renal injury frequently emerges within 48 hours of admission. Independent predictors of AKI included inotrope use within 24 h (OR 9.6, p=0.005), NSAID exposure (OR 3.0, p=0.003), transfusion burden (FFP OR 1.15 per unit, p=0.022; RBC OR 1.15 per unit, p=0.029), higher lactate (OR 1.77, p=0.012), and lower diuresis (OR 0.15, p=0.002). Mannitol appeared to amplify AKI risk in elderly, highly catabolic patients or in those with rhabdomyolysis (creatine kinase ≥5,000 U/L. Organ dysfunction metrics were informative: a maximum SOFA score≥9 showed 84% specificity for predicting ICU mortality (AUC 0.71), while SOFA amplitude demonstrated excellent discrimination (AUC 0.87). Inflammatory dynamics paralleled hemodynamic stress: neutrophil-to-lymphocyte ratio (NLR) amplitude was independently associated with AKI (OR 1.04, p=0.044) and often overlapped with declining urinary sodium, suggesting coupled hemodynamic–inflammatory injury.

AKI was strongly associated with mortality (75.8% vs 29.9% without AKI, p<0.001). After adjustment for age, sex, hypertension, mean arterial pressure, lactate, bicarbonate, hemoglobin, creatine kinase, and Injury Severity Score, AKI remained an independent predictor of ICU death (aOR 6.44; 95% CI 2.54–16.35; p<0.0001).[Figure1]

In this cohort, early hemodynamic stress and treatment exposures primarily signaled risk for AKI, while AKI itself was the dominant determinant of ICU mortality. Bedside signals available on Day 1: inotropes, NSAIDs, transfusions, lactate, and urine output identify high-risk patients for AKI, while SOFA amplitude adds prognostic granularity beyond single-time-point scores. These findings support care strategies that prioritize early hemodynamic optimization, parsimonious use of nephrotoxins and blood products, and close monitoring of organ-dysfunction dynamics, with the explicit goal of preventing or rapidly reversing AKI to improve survival.

Funding:This research is part of the project funded by the National Agency for Scientific Research and Innovation (NASRI), Albania.