Association between albumin-corrected anion gap and adverse outcomes in patients with acute exacerbation of chronic obstructive pulmonary disease in the intensive care unit

Background The albumin-corrected anion gap (ACAG) has been linked to prognosis in various diseases, but its predictive value in acute exacerbation of chronic obstructive pulmonary disease (AECOPD) remains inadequately explored. This study aims to examine the association between ACAG levels and adverse clinical outcomes in AECOPD patients admitted to the intensive care unit (ICU). Methods This retrospective cohort study used data from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. Adult patients diagnosed with AECOPD and admitted to the ICU were included. Patients were categorized into quartiles based on ACAG levels. Primary outcomes were all-cause mortality at 30 and 365 days. Secondary outcomes included in-hospital mortality, mechanical ventilation, ICU readmission, and the length of ICU and hospital stay. Kaplan–Meier survival curves, Cox proportional hazards models, and restricted cubic spline (RCS) analyses were utilized to assess the relationship between ACAG and adverse outcomes. The incremental prognostic value of ACAG over the traditional anion gap and the Sequential Organ Failure Assessment (SOFA) score was also evaluated. Results A total of 585 AECOPD patients were included in the study. The all-cause mortality rates at 30 days, 365 days, and in-hospital mortality rates were 25.4% ( n = 149), 46.4% ( n = 272), and 16.5% ( n = 97), respectively. Kaplan–Meier analyses showed significant differences in 30-day and 365-day survival across ACAG quartiles. After full adjustment, higher ACAG remained associated with 30-day mortality both as a continuous variable (HR per 1 mmol/L, 1.054; 95% CI, 1.008–1.101; P = 0.020) and as a categorical variable (Q4 vs. Q1: HR, 1.922; 95% CI, 1.140–3.242; P = 0.015). However, the fully adjusted associations with 365-day mortality (HR per 1 mmol/L, 1.015; 95% CI, 0.983–1.049; P = 0.353) and in-hospital mortality (OR, 1.062; 95% CI, 0.997–1.132; P = 0.063) were not statistically significant. RCS analyses revealed no evidence of nonlinear associations between ACAG and mortality. Piecewise Cox analyses indicated that the association was concentrated during the early follow-up period. ACAG showed better discrimination than the traditional anion gap for 30-day mortality, whereas its incremental contribution beyond SOFA was modest. Conclusions Elevated ACAG was independently associated with increased 30-day all-cause mortality in ICU patients with AECOPD, with the association most pronounced during early follow-up. However, its associations with 365-day and in-hospital mortality were attenuated after comprehensive adjustment, and its incremental prognostic value was modest. ACAG may serve as an adjunctive marker for early risk stratification but should not be regarded as a standalone prognostic tool. Clinical trial number Not applicable.