WCN26-7159 原発性副腎不全による急性腎障害:2件の症例報告

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.Methods: 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.Results: 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. p<0.0001).[Figure1]Conclusion: 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.