Abstract

Sepsis-associated acute kidney injury (S-AKI) presents significant clinical challenges, necessitating deeper insights into its molecular mechanisms. We conducted a comprehensive analysis—including Principal Component Analysis (PCA), differential gene expression, KEGG pathway enrichment, and Gene Set Enrichment Analysis (GSEA)—to elucidate the underlying pathways involved in S-AKI. PCA revealed distinct clustering between S-AKI patients and controls, with differential gene expression identifying 1,759 significant genes (912 upregulated, 847 downregulated). Notable upregulated genes included CYP19A1 and LY6G6F, while downregulated genes encompassed LRP1B and SIGLEC8. KEGG analysis highlighted pathways related to adaptive immune responses and infection, such as “Th1 and Th2 cell differentiation" and "Primary immunodeficiency.” GSEA pinpointed "Neutrophil extracellular trap formation" as the most significantly enriched pathway, underscoring neutrophil-mediated responses in S-AKI. Our findings suggest potential molecular targets for diagnosis and therapeutic intervention, providing a foundation for future research and improved clinical outcomes.

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