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Introduction <p>To investigate the early predictive value of serum histone deacetylase 3 (HDAC3) levels for sepsis-associated acute kidney injury (SA-AKI) and evaluate its ability to differentiate between various stages of acute kidney injury (AKI).</p> Methods <p>A prospective cohort study was conducted among patients with sepsis admitted to the intensive care unit (ICU) of Yancheng First People’s Hospital between January 2025 and October 2025. All participants met the Sepsis-3 diagnostic criteria and had no AKI at ICU admission. Patients were stratified according to the development of AKI within seven days after diagnosis, and AKI severity was staged using KDIGO guidelines. Multivariable logistic regression was used to identify independent risk factors for SA-AKI. Receiver operating characteristic (ROC) curves were generated to assess the predictive performance of HDAC3 and related biomarkers. Subgroup analysis evaluated the discriminatory ability of HDAC3 between mild (KDIGO stage 1) and severe AKI (KDIGO stages 2–3). Kaplan–Meier survival analysis was performed to examine the association between HDAC3 levels and 28-day survival.</p> Results <p>A total of 90 patients with sepsis were enrolled, of whom 50 (55.6%) developed AKI within seven days. Patients with SA-AKI exhibited significantly higher SOFA scores, APACHE II scores, PCT, CRP, and serum HDAC3 levels than those without AKI (<i>P</i> &lt; 0.05). Multivariable analysis identified SOFA score, CRP, PCT, and serum HDAC3 as independent risk factors for SA-AKI. ROC analysis showed that HDAC3 achieved an AUC of 0.820 (95% CI: 0.732–0.908), which was higher than those of SOFA, CRP, and PCT. Serum HDAC3 levels showed a significant stepwise increase across KDIGO stages, and stratified analysis demonstrated an AUC of 0.828 (95% CI: 0.694–0.920) for distinguishing mild from severe AKI. Higher HDAC3 levels were also significantly associated with reduced 28-day survival (log-rank <i>P</i> &lt; 0.05).</p> Conclusion <p>Elevated serum HDAC3 levels are associated with the development, severity, and prognosis of SA-AKI. While these findings provide supportive evidence for the potential role of HDAC3 in early risk stratification and AKI staging, validation in larger, multi-center cohorts is required to confirm its clinical utility.</p>

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Serum HDAC3 as an early biomarker for prediction and staging of sepsis-associated AKI: prospective cohort study

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月5日

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  • Wei-ying Liu,
  • Min Chen,
  • Dong-yu Chen,
  • Xing Li,
  • Bo Xi,
  • Fang Chen,
  • Yi-jun Deng

摘要

Introduction

To investigate the early predictive value of serum histone deacetylase 3 (HDAC3) levels for sepsis-associated acute kidney injury (SA-AKI) and evaluate its ability to differentiate between various stages of acute kidney injury (AKI).

Methods

A prospective cohort study was conducted among patients with sepsis admitted to the intensive care unit (ICU) of Yancheng First People’s Hospital between January 2025 and October 2025. All participants met the Sepsis-3 diagnostic criteria and had no AKI at ICU admission. Patients were stratified according to the development of AKI within seven days after diagnosis, and AKI severity was staged using KDIGO guidelines. Multivariable logistic regression was used to identify independent risk factors for SA-AKI. Receiver operating characteristic (ROC) curves were generated to assess the predictive performance of HDAC3 and related biomarkers. Subgroup analysis evaluated the discriminatory ability of HDAC3 between mild (KDIGO stage 1) and severe AKI (KDIGO stages 2–3). Kaplan–Meier survival analysis was performed to examine the association between HDAC3 levels and 28-day survival.

Results

A total of 90 patients with sepsis were enrolled, of whom 50 (55.6%) developed AKI within seven days. Patients with SA-AKI exhibited significantly higher SOFA scores, APACHE II scores, PCT, CRP, and serum HDAC3 levels than those without AKI (P < 0.05). Multivariable analysis identified SOFA score, CRP, PCT, and serum HDAC3 as independent risk factors for SA-AKI. ROC analysis showed that HDAC3 achieved an AUC of 0.820 (95% CI: 0.732–0.908), which was higher than those of SOFA, CRP, and PCT. Serum HDAC3 levels showed a significant stepwise increase across KDIGO stages, and stratified analysis demonstrated an AUC of 0.828 (95% CI: 0.694–0.920) for distinguishing mild from severe AKI. Higher HDAC3 levels were also significantly associated with reduced 28-day survival (log-rank P < 0.05).

Conclusion

Elevated serum HDAC3 levels are associated with the development, severity, and prognosis of SA-AKI. While these findings provide supportive evidence for the potential role of HDAC3 in early risk stratification and AKI staging, validation in larger, multi-center cohorts is required to confirm its clinical utility.