Impact of diabetes mellitus and glucose level control on early sepsis-associated acute kidney injury: a multicenter retrospective observational study.
Sepsis-associated acute kidney injury (SA-AKI) raises mortality risk, while the independent links of pre-existing diabetes mellitus (DM) and in-hospital glycemic status to SA-AKI remain unclear. This study explored their correlations with early SA-AKI among sepsis patients.
This multicenter retrospective cohort enrolled 6,974 pathogen-positive adult sepsis patients admitted to ICUs from 2023 to 2026. We used pre-existing DM as the primary exposure and time-weighted average glucose as the secondary marker. Multiple adjustment methods including propensity score matching (PSM) and inverse probability weighting (IPW) were adopted to reduce confounding bias.
After enrolling 6,947 septic ICU patients, multivariate logistic regression identified pre-existing DM as an independent risk factor for early SA-AKI (adjusted OR = 2.54, 95% CI 2.25-2.86, p < 0.001). The protective glycemic range was 6-11 mmol/L for diabetic patients (adjusted OR = 0.88, 95% CI 0.78-0.98, p = 0.025) and 8-13 mmol/L for non-diabetic patients (adjusted OR = 0.55, 95% CI 0.48-0.62, p < 0.001). PSM, IPW and doubly robust estimation all validated these consistent associations. Abnormal glucose showed weak predictive power for SA-AKI (AUC 0.60-0.61). Higher time-weighted glucose correlated with advanced AKI stages and increased in-hospital mortality in mild-to-moderate SA-AKI patients. Diabetic SA-AKI patients had higher proportions of stage 1 and stage 3 AKI without significant difference in overall in-hospital mortality compared with non-diabetic counterparts. Matched SA-AKI patients suffered longer ICU/hospital stays, more organ support use and higher hospital mortality.
Common pathogenic organisms had higher detection rates in SA-AKI cases. Pre-existing DM was positively correlated with early SA-AKI. Targeted in-hospital glycemic intervals were linked to lower SA-AKI risk, which supports individualized glucose monitoring for sepsis patients.
This multicenter retrospective cohort enrolled 6,974 pathogen-positive adult sepsis patients admitted to ICUs from 2023 to 2026. We used pre-existing DM as the primary exposure and time-weighted average glucose as the secondary marker. Multiple adjustment methods including propensity score matching (PSM) and inverse probability weighting (IPW) were adopted to reduce confounding bias.
After enrolling 6,947 septic ICU patients, multivariate logistic regression identified pre-existing DM as an independent risk factor for early SA-AKI (adjusted OR = 2.54, 95% CI 2.25-2.86, p < 0.001). The protective glycemic range was 6-11 mmol/L for diabetic patients (adjusted OR = 0.88, 95% CI 0.78-0.98, p = 0.025) and 8-13 mmol/L for non-diabetic patients (adjusted OR = 0.55, 95% CI 0.48-0.62, p < 0.001). PSM, IPW and doubly robust estimation all validated these consistent associations. Abnormal glucose showed weak predictive power for SA-AKI (AUC 0.60-0.61). Higher time-weighted glucose correlated with advanced AKI stages and increased in-hospital mortality in mild-to-moderate SA-AKI patients. Diabetic SA-AKI patients had higher proportions of stage 1 and stage 3 AKI without significant difference in overall in-hospital mortality compared with non-diabetic counterparts. Matched SA-AKI patients suffered longer ICU/hospital stays, more organ support use and higher hospital mortality.
Common pathogenic organisms had higher detection rates in SA-AKI cases. Pre-existing DM was positively correlated with early SA-AKI. Targeted in-hospital glycemic intervals were linked to lower SA-AKI risk, which supports individualized glucose monitoring for sepsis patients.
Authors
Zhao Zhao, Cui Cui, Dong Dong, Wang Wang, Yang Yang, Wang Wang, Shi Shi, Shi Shi, Cao Cao, Chen Chen, Wang Wang, Li Li
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