Association of Causative Pathogens With Acute Kidney Injury in Adult Patients With Community-Onset Sepsis

社区获得性脓毒症成人患者急性肾损伤与致病病原体的关联

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Abstract

IMPORTANCE: The influence of disease-causing pathogen on acute kidney injury (AKI) in septic patients is poorly understood. OBJECTIVES: We examined the association of microbial pathogen with AKI among patients with community-onset sepsis. DESIGN, SETTING, AND PARTICIPANTS: This was a retrospective cohort study. Patient data were acquired from the nationwide multicenter PINC AI Healthcare Database (2016-2020). Participants included adult patients with Centers for Disease Control and Prevention-defined community-onset sepsis. MAIN OUTCOMES AND MEASURES: The primary exposure was pathogen type identified by culture growth. Microbial cultures from any site were included. The primary endpoint was development of AKI within 7 days of admission using the Kidney Disease: Improving Global Outcomes serum creatinine criteria. We used multilevel logistic regression to examine the association between pathogen type and AKI. Escherichia coli-positive cultures were used as the reference category. RESULTS: We included 119,733 patients with community-onset sepsis. The median age was 67 years, 33.3% were mechanically ventilated, 36.1% received vasopressors, and hospital mortality was 13.1%. Forty-two thousand twenty-seven patients (35.1%) developed stage 1 AKI, 22,979 (19.2%) developed stage 2 AKI, and 25,073 (20.9%) developed stage 3 AKI. Relative to patients with E. coli infection (odds ratio [OR], 1.0), Proteus species (OR, 1.26; 95% CI, 1.06-1.50), and Streptococcus species (OR, 1.24; 95% CI, 1.10-1.41) were associated with increased odds of AKI. Meanwhile, Pseudomonas aeruginosa (OR, 0.56; 95% CI, 0.49-0.64) and Serratia species (OR, 0.70; 95% CI, 0.52-0.94) were associated with decreased odds of AKI. CONCLUSIONS AND RELEVANCE: The causative pathogen in patients with sepsis may influence the development of AKI. Further mechanistic and clinical research is needed to confirm these findings and to explore how different pathogens may affect AKI risk in critically ill patients.

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