Background: Acute kidney injury (AKI) refers to a sudden loss of renal function. This study was performed to identify the key RNAs acting in the mechanism of sepsis-induced AKI.Methods: Microarray dataset GSE94717 (including six sepsis-induced AKI samples and three control samples) was downloaded from Gene Expression Omnibus database. Differentially expressed miRNAs (DE-miRNAs) were identified. The miRNA targets were predicted and enrichment analysis was performed. Protein-protein interaction (PPI) and competing endogenous RNA (ceRNA) regulatory networks were constructed. Mouse podocytes were treated with lipopolysaccharide (LPS), following by cell viability and PCR analysis. Cellular apoptosis and the ceRNA network were validated.Results: Thirty-one common DE-miRNAs (two up-regulated and 29 down-regulated) by AKI versus control and male AKI versus control were identified. We found the targets of miR-15a-5p, miR-15b-5p, and miR-16-5p were involved in mTOR signaling pathway, and those of miR-29b-3p and miR-16-5p were enriched in PI3K-Akt signaling pathway. RNAs including miR-15b-5p, miR-15a-5p, miR-107, XIST, miR-16-5p, and cullin 3 gene (CUL3) were included in the ceRNA regulatory network. The downregulation of miR-15a-5p and miR-15b-5p and the upregulation of lncRNA XIST and CUL3 gene were validated using qPCR. The miR-15a-5p-XIST-CUL3 regulatory axis was identified and was validated. We confirmed that LPS inhibited the growth of mouse podocytes and seven of the ten miRNAs, but upregulated XIST and CUL3. Transfection analysis showed XIST siRNA enhanced LPS-induced MPC5 cell apoptosis and miR-15a-5p inhibitor reserved it, so did as CUL3 overexpression for miR-15a-5p mimics.Conclusion: The miR-15a-5p-XIST-CUL3 regulatory axis was related to the pathogenesis of sepsis-induced AKI.HighlightsTotally, 31 miRNAs were dysregulated between disease and control groups.MiR-15a-5p, miR-15b-5p, and miR-16-5p were involved in mTOR signaling pathway.MiR-16-5p and miR-29b-3p were implicated in PI3K-Akt signaling pathway.The miR-15a-5p-XIST-CUL3 axis was critical for sepsis-induced AKI.

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Objective Inflammation can cause delirium. Soluble fibrinogen‐like protein 2 (sFGL2) is a modulator of the immune response and more recently found to be a biomarker for brain injury. This study was designed to discover the predictive capability of serum sFGL2 concentrations for delirium after acute pancreatitis (AP). Materials and Methods In this prospective, observational study, serum sFGL2 concentrations were quantified in 184 healthy controls and in 184 AP patients. Disease severity was assessed by Acute Physiology and Chronic Health Care Evaluation II score, Ranson score, multiple organ dysfunction score, and sequential organ failure assessment score. Delirium was recorded during hospital stay. Predictors of delirium were identified using multivariate analysis. Results Serum sFGL2 concentrations were substantially higher in AP patients than in controls. Serum sFGL2 concentrations were intimately correlated with the preceding severity parameters. Serum sFGL2 and the aforementioned severity parameters were independent predictors for delirium. Under receiver operating characteristic curve, the discriminatory ability of serum sFGL2 was equivalent to those of the above‐mentioned severity parameters. Moreover, serum sFGL2 dramatically improved the predictive value of the aforementioned severity parameters. Conclusions Elevation of serum sFGL2 concentrations is strongly associated with the AP severity and has the potential to distinguish delirium after AP.

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