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<p>Sepsis-associated acute kidney injury (SA-AKI) is categorized into transient AKI (<i>t</i>-AKI; recovery within 48&#xa0;h) and persistent AKI (<i>p</i>-AKI; impairment &gt; 48&#xa0;h). Early identification of high-risk patients is essential for improving outcomes. This study assessed whether albumin-corrected anion gap (ACAG) predicts p-AKI progression in SA-AKI patients. This retrospective cohort study was conducted using data from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. Consecutive patients with SA-AKI admitted to the intensive care unit (ICU) for the first time were enrolled. The dose-response relationship between ACAG levels and the development of <i>p</i>-AKI was explored using restricted cubic splines (RCS). Multivariable logistic regression models were fitted to assess the independent association of ACAG with persistent AKI. Subgroup analyses were performed to examine the robustness of the findings. A total of 6759 patients with sepsis-associated SA-AKI were included in the final analysis, among whom 3,656 (54.09%) experienced progression to <i>p</i>-AKI during the observation period. Using RCS with four knots placed at the 5th, 35th, 65th, and 95th percentiles, we identified a significant linear relationship between ACAG levels and the probability of <i>p</i>-AKI development. Multivariable logistic regression analysis demonstrated that elevated ACAG levels were independently associated with progression to <i>p</i>-AKI in patients with SA-AKI. Using a cutoff value of 20.63 mmol/L determined by maximizing the Youden index, patients with ACAG ≥ 20.63 mmol/L exhibited a significantly increased risk of <i>p</i>-AKI compared with those with lower levels (aOR 2.78; 95% CI, 2.51–3.09) in the fully adjusted model. Elevated ACAG levels are independently associated with an increased risk of progression to <i>p</i>-AKI in patients with SA-AKI, suggesting that ACAG may serve as a potential biomarker for early identification of high-risk individuals. </p>

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Association between albumin corrected anion gap and persistent acute kidney injury in patients with sepsis-associated acute kidney injury: a retrospective study based on the MIMIC-IV database

  • 期刊论文

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  • 发表日期：

    2026年7月22日

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  • Jie Sun,
  • Chaojun Cai,
  • Yan Wang,
  • Lu Pei

摘要

Sepsis-associated acute kidney injury (SA-AKI) is categorized into transient AKI (t-AKI; recovery within 48 h) and persistent AKI (p-AKI; impairment > 48 h). Early identification of high-risk patients is essential for improving outcomes. This study assessed whether albumin-corrected anion gap (ACAG) predicts p-AKI progression in SA-AKI patients. This retrospective cohort study was conducted using data from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. Consecutive patients with SA-AKI admitted to the intensive care unit (ICU) for the first time were enrolled. The dose-response relationship between ACAG levels and the development of p-AKI was explored using restricted cubic splines (RCS). Multivariable logistic regression models were fitted to assess the independent association of ACAG with persistent AKI. Subgroup analyses were performed to examine the robustness of the findings. A total of 6759 patients with sepsis-associated SA-AKI were included in the final analysis, among whom 3,656 (54.09%) experienced progression to p-AKI during the observation period. Using RCS with four knots placed at the 5th, 35th, 65th, and 95th percentiles, we identified a significant linear relationship between ACAG levels and the probability of p-AKI development. Multivariable logistic regression analysis demonstrated that elevated ACAG levels were independently associated with progression to p-AKI in patients with SA-AKI. Using a cutoff value of 20.63 mmol/L determined by maximizing the Youden index, patients with ACAG ≥ 20.63 mmol/L exhibited a significantly increased risk of p-AKI compared with those with lower levels (aOR 2.78; 95% CI, 2.51–3.09) in the fully adjusted model. Elevated ACAG levels are independently associated with an increased risk of progression to p-AKI in patients with SA-AKI, suggesting that ACAG may serve as a potential biomarker for early identification of high-risk individuals.