Renal failure · 2025
Systemic immune-inflammatory biomarkers assist in differentiating clinical features of different etiologies of acute kidney injury: results from eICU Collaborative Research Database.
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Liang Qiqiang, Zhang Sumian, Wang Xuebin
Аннотация
BACKGROUND: The relationship between distinct etiologies of acute kidney injury (AKI) and systemic immune-inflammatory biomarkers remains poorly defined.
METHODS: We performed a retrospective cohort study utilizing the eICU Collaborative Research Database (eICU-CRD), a multicenter U.S. dataset. The study included all patients diagnosed with AKI while excluding those with unclear AKI etiology or chronic kidney disease. Analyzed variables encompassed demographic characteristics, admission/discharge data, laboratory parameters, severity scores, and comorbidities. We specifically evaluated four clinically accessible systemic immune-inflammatory indices. Intergroup differences were assessed using letter notations, nonlinear relationships were explored via restricted cubic spline models, and confounding variables were controlled for using propensity score matching.
RESULTS: The analysis included 2,912 patients with AKI of known etiology, categorized into six etiological subgroups. Pairwise comparisons revealed significant differences (p < 0.001) in systemic immune-inflammatory biomarkers between a high-inflammation group (sepsis-associated AKI, acute tubular necrosis [ATN], hepatorenal syndrome) and other subgroups (hypovolemic, obstructive, ischemic, and drug-induced AKI). Notable disparities emerged for the systemic immune-inflammation index (SII) (4,120 vs. 3,340) and neutrophil-to-lymphocyte ratio (NLR) (19.1 vs. 14.7). Cox regression identified independent predictors of mortality: membership in the high-inflammation group (Odds Ratio [OR] = 1.67, 95% Confidence Interval [CI] = 1.39-2.00) and septic shock (OR = 1.65, 95% CI = 1.46-1.84). Following propensity score matching, the high-inflammation group remained a significant independent risk factor for mortality.
CONCLUSION: Patients with AKI primarily attributed to sepsis, ATN, or hepatorenal syndrome constitute a high-inflammation subgroup characterized by elevated systemic immune-inflammatory biomarkers. This subgroup independently predicts increased mortality risk.
METHODS: We performed a retrospective cohort study utilizing the eICU Collaborative Research Database (eICU-CRD), a multicenter U.S. dataset. The study included all patients diagnosed with AKI while excluding those with unclear AKI etiology or chronic kidney disease. Analyzed variables encompassed demographic characteristics, admission/discharge data, laboratory parameters, severity scores, and comorbidities. We specifically evaluated four clinically accessible systemic immune-inflammatory indices. Intergroup differences were assessed using letter notations, nonlinear relationships were explored via restricted cubic spline models, and confounding variables were controlled for using propensity score matching.
RESULTS: The analysis included 2,912 patients with AKI of known etiology, categorized into six etiological subgroups. Pairwise comparisons revealed significant differences (p < 0.001) in systemic immune-inflammatory biomarkers between a high-inflammation group (sepsis-associated AKI, acute tubular necrosis [ATN], hepatorenal syndrome) and other subgroups (hypovolemic, obstructive, ischemic, and drug-induced AKI). Notable disparities emerged for the systemic immune-inflammation index (SII) (4,120 vs. 3,340) and neutrophil-to-lymphocyte ratio (NLR) (19.1 vs. 14.7). Cox regression identified independent predictors of mortality: membership in the high-inflammation group (Odds Ratio [OR] = 1.67, 95% Confidence Interval [CI] = 1.39-2.00) and septic shock (OR = 1.65, 95% CI = 1.46-1.84). Following propensity score matching, the high-inflammation group remained a significant independent risk factor for mortality.
CONCLUSION: Patients with AKI primarily attributed to sepsis, ATN, or hepatorenal syndrome constitute a high-inflammation subgroup characterized by elevated systemic immune-inflammatory biomarkers. This subgroup independently predicts increased mortality risk.