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Purpose <p>Sepsis-Associated Acute Kidney Injury (SA-AKI) is a major complication in critically ill patients, yet early predictive biomarkers remain limited. Given the interplay between coagulation, inflammation, and microcirculatory dysfunction in SA-AKI pathogenesis. This study aimed to evaluate the association between platelet-to-hemoglobin ratio (PHR) and SA-AKI development in multicenter intensive care unit (ICU) cohorts.</p> Methods <p>We extracted patient data from the Medical Information Mart for Intensive Care IV (MIMIC-IV) and electronic Intensive Care Unit (eICU) databases. Based on Kidney Disease: Improving Global Outcomes (KDIGO) criteria, patients were stratified into AKI (<i>n</i> = 4,825) and non-AKI (<i>n</i> = 3,390) cohorts. Multiple statistical approaches—including multivariable logistic regression, propensity score matching (PSM), and inverse probability weighting (IPW)—were employed to adjust for confounders. The primary outcome was SA-AKI incidence.</p> Results <p>Elevated PHR was consistently associated with increased SA-AKI risk. In the adjusted logistic regression model, PHR remained independently predictive (OR 1.06, 95% CI: 1.05–1.07; <i>P</i> &lt; 0.001). This association was validated through PSM (OR 1.12, 95% CI: 1.11–1.13; <i>P</i> &lt; 0.001) and IPW (OR 1.03, 95% CI: 1.02–1.03; <i>P</i> &lt; 0.001). The incidence of AKI significantly increases when PHR &gt; 20. Generalized additive model (GAM) analysis revealed a linear correlation between PHR &gt; 22 and SA-AKI mortality (<i>P</i> &lt; 0.001), though PHR showed no significant association with AKI severity (<i>P</i> = 0.029). Our study demonstrates that the emerging biomarker PHR alone achieved an AUC of 0.845 for prognostic prediction and 0.584 for diagnostic performance. When combined with SOFA and SAPS-II, the prognostic model (Model 4) significantly improved (AUC = 0.906 and 0.713), outperforming individual components.</p> Conclusions <p>PHR demonstrates a statistically significant association with SA-AKI risk in our analyses, its modest discriminative capacity highlights its role as a complementary rather than standalone predictor. These findings support further validation of PHR as a pragmatic biomarker to identify high-risk sepsis patients who may benefit from intensified hemodynamic or coagulation monitoring.</p> Clinical trial number <p>Not applicable.</p>

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Platelet-to-hemoglobin ratio as a novel prognostic biomarker in sepsis-associated AKI: a multicenter cohort study

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月25日

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  • Lina Zhao,
  • Qing Zhang,
  • Zheng Li,
  • Yuehao Shen,
  • Dongxue Huang,
  • Haiying Liu,
  • Xuguang Li,
  • Qinghe Yan,
  • Yun Li,
  • Yuan Yuan,
  • Keliang Xie

摘要

Purpose

Sepsis-Associated Acute Kidney Injury (SA-AKI) is a major complication in critically ill patients, yet early predictive biomarkers remain limited. Given the interplay between coagulation, inflammation, and microcirculatory dysfunction in SA-AKI pathogenesis. This study aimed to evaluate the association between platelet-to-hemoglobin ratio (PHR) and SA-AKI development in multicenter intensive care unit (ICU) cohorts.

Methods

We extracted patient data from the Medical Information Mart for Intensive Care IV (MIMIC-IV) and electronic Intensive Care Unit (eICU) databases. Based on Kidney Disease: Improving Global Outcomes (KDIGO) criteria, patients were stratified into AKI (n = 4,825) and non-AKI (n = 3,390) cohorts. Multiple statistical approaches—including multivariable logistic regression, propensity score matching (PSM), and inverse probability weighting (IPW)—were employed to adjust for confounders. The primary outcome was SA-AKI incidence.

Results

Elevated PHR was consistently associated with increased SA-AKI risk. In the adjusted logistic regression model, PHR remained independently predictive (OR 1.06, 95% CI: 1.05–1.07; P < 0.001). This association was validated through PSM (OR 1.12, 95% CI: 1.11–1.13; P < 0.001) and IPW (OR 1.03, 95% CI: 1.02–1.03; P < 0.001). The incidence of AKI significantly increases when PHR > 20. Generalized additive model (GAM) analysis revealed a linear correlation between PHR > 22 and SA-AKI mortality (P < 0.001), though PHR showed no significant association with AKI severity (P = 0.029). Our study demonstrates that the emerging biomarker PHR alone achieved an AUC of 0.845 for prognostic prediction and 0.584 for diagnostic performance. When combined with SOFA and SAPS-II, the prognostic model (Model 4) significantly improved (AUC = 0.906 and 0.713), outperforming individual components.

Conclusions

PHR demonstrates a statistically significant association with SA-AKI risk in our analyses, its modest discriminative capacity highlights its role as a complementary rather than standalone predictor. These findings support further validation of PHR as a pragmatic biomarker to identify high-risk sepsis patients who may benefit from intensified hemodynamic or coagulation monitoring.

Clinical trial number

Not applicable.