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<p>Sepsis-associated acute kidney injury (SA-AKI) commonly affects critically ill patients, but its early detection remains difficult. Biomarkers that facilitate early detection of patients susceptible to SA-AKI remain essential. This investigation seeks to evaluate the independent association between early serum S100A8/A9 levels and SA-AKI, considering 28-day all-cause mortality as a secondary endpoint. This single-center observational cohort investigation employed a hybrid (ambidirectional) design, enrolling 211 adult sepsis patients per the Sepsis-3 criteria. Among them, 118 developed SA-AKI within 7&#xa0;days, while 93 did not. Serum S100A8/A9 levels were assessed within 2&#xa0;h of intensive care unit (ICU) admission and again on days 1, 3, and 7. Demographic, clinical, and laboratory data were gathered. Multivariable logistic regression and restricted cubic spline analyses assessed the independent relationship between S100A8/A9 at ICU admission and SA-AKI, and receiver operating characteristic curves evaluated its discriminatory ability. Generalized estimating equations were utilized to compare longitudinal S100A8/A9 changes between groups, while Cox proportional hazards models evaluated the connection between S100A8/A9 and 28-day all-cause mortality. Serum S100A8/A9 levels within 2&#xa0;h of ICU admission demonstrated significant elevation in patients developing SA-AKI versus those without AKI [3981.9 (3355.5, 5007.9) pg/mL vs. 3411.8 (2781.5, 3922.5) pg/mL; <i>P</i> &lt; 0.001] and remained elevated on days 1, 3, and 7, despite an overall decline. Generalized estimating equation analysis revealed significant time and group effects (both <i>P</i> &lt; 0.001). At ICU admission, S100A8/A9 was independently associated with SA-AKI (adjusted OR 1.13 per 100&#xa0;pg/mL; 95% CI 1.08–1.19; <i>P</i> &lt; 0.001), with restricted cubic spline analysis indicating an approximately linear relationship. The area under the curve of S100A8/A9 at ICU admission for identifying SA-AKI was 0.721 (95% CI 0.653–0.788), with optimal threshold at 3732.1&#xa0;pg/mL (sensitivity 61.9%, specificity 68.8%). The combined model (SOFA + S100A8/A9) demonstrated enhanced discrimination relative to SOFA alone (area under the curve 0.861 <i>vs.</i> 0.771; DeLong <i>P</i> = 0.0001). In Cox models, S100A8/A9 showed no independent link to 28-day all-cause mortality. Elevated serum S100A8/A9 levels were independently associated with SA-AKI, but no independent link to 28-day all-cause mortality was observed.</p>

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Association of serum S100A8/A9 with sepsis-associated acute kidney injury and 28-day mortality: a hybrid cohort study

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月30日

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  • Yanan Lv,
  • Mengjia Yu,
  • Yumei Mao,
  • Feng Qu,
  • Qingjie Xue,
  • Huanqin Liu,
  • Jikui Shi

摘要

Sepsis-associated acute kidney injury (SA-AKI) commonly affects critically ill patients, but its early detection remains difficult. Biomarkers that facilitate early detection of patients susceptible to SA-AKI remain essential. This investigation seeks to evaluate the independent association between early serum S100A8/A9 levels and SA-AKI, considering 28-day all-cause mortality as a secondary endpoint. This single-center observational cohort investigation employed a hybrid (ambidirectional) design, enrolling 211 adult sepsis patients per the Sepsis-3 criteria. Among them, 118 developed SA-AKI within 7 days, while 93 did not. Serum S100A8/A9 levels were assessed within 2 h of intensive care unit (ICU) admission and again on days 1, 3, and 7. Demographic, clinical, and laboratory data were gathered. Multivariable logistic regression and restricted cubic spline analyses assessed the independent relationship between S100A8/A9 at ICU admission and SA-AKI, and receiver operating characteristic curves evaluated its discriminatory ability. Generalized estimating equations were utilized to compare longitudinal S100A8/A9 changes between groups, while Cox proportional hazards models evaluated the connection between S100A8/A9 and 28-day all-cause mortality. Serum S100A8/A9 levels within 2 h of ICU admission demonstrated significant elevation in patients developing SA-AKI versus those without AKI [3981.9 (3355.5, 5007.9) pg/mL vs. 3411.8 (2781.5, 3922.5) pg/mL; P < 0.001] and remained elevated on days 1, 3, and 7, despite an overall decline. Generalized estimating equation analysis revealed significant time and group effects (both P < 0.001). At ICU admission, S100A8/A9 was independently associated with SA-AKI (adjusted OR 1.13 per 100 pg/mL; 95% CI 1.08–1.19; P < 0.001), with restricted cubic spline analysis indicating an approximately linear relationship. The area under the curve of S100A8/A9 at ICU admission for identifying SA-AKI was 0.721 (95% CI 0.653–0.788), with optimal threshold at 3732.1 pg/mL (sensitivity 61.9%, specificity 68.8%). The combined model (SOFA + S100A8/A9) demonstrated enhanced discrimination relative to SOFA alone (area under the curve 0.861 vs. 0.771; DeLong P = 0.0001). In Cox models, S100A8/A9 showed no independent link to 28-day all-cause mortality. Elevated serum S100A8/A9 levels were independently associated with SA-AKI, but no independent link to 28-day all-cause mortality was observed.