The predictive performance of the lactate clearance rate combined with the APACHE II score in the prediction of sepsis-associated acute kidney injury in 7 days.

Background: The purpose of this study was to evaluate the accuracy of the lactate clearance rate (LCR) combined with the Acute Physiology and Chronic Health Evaluation II (APACHE II) score in the prediction of sepsis-associated acute kidney injury (SAKI). Methods: Sepsis patients were divided into the SAKI group and non-SAKI group. Arterial blood lactate was collected at 0 h (before treatment), 2 h, 4 h, 6 h, and 8 h (after treatment), and the LCR was calculated. The physiological parameters and laboratory test results were used to calculate the APACHE II score and the Sequential Organ Failure Assessment (SOFA) score. The receiver operating characteristic (ROC) curves of LCR, APACHE II score and SOFA score for predicting patients with SAKI were drawn. Two single indicators with high areas under the curves (AUCs) were selected to calculate the joint probability through regression analysis, and the prediction efficiency corresponding to each curve was analyzed. Results: There were significant differences in LCR between different groups and time periods (Fgroup=17.44, Pgroup ≤0.0001, Ftime =11.71, Ptime =0.0014). After 8 h of treatment, there was a significant difference in the overall compliance rate between the 2 groups (P<0.0001). In addition, after 24 h of treatment, the APACHE II score in the SAKI group was significantly higher than that in the non-SAKI group (P=0.0007), and SOFA score was also significantly higher than that in the non-SAKI group (P=0.0001). ROC curve showed that the 0-8 h LCR and APACHE II scores had a high predictive performance for the acute kidney injury (AKI) occurrence in sepsis patients, and AUCs were 0.7637 and 0.7517, respectively, while the combined AUC of the 2 indicators was 0.7975. Conclusions: The 0-8 h LCR combined with APACHE II score can improve the early predictive value of SAKI, reduce the risk of AKI in patients with sepsis/septic shock, and reduce the social and family burden, which is worthy of clinical application.

MiR-106a aggravates sepsis-induced acute kidney injury by targeting THBS2 in mice model.

PURPOSE: To investigate the role and related mechanisms of miR-106a in sepsis-induced AKI. METHODS: Serum from sepsis and healthy patients was collected, sepsis mouse model was established by cecal ligation and puncture (CLP). TCMK-1 cells were treated with lipopolysaccharide (LPS) and transfected with THBS2-small interfering RNA (siTHBS2), miR-106a inhibitor, miR-106a mimics and their negative controls (NCs). The expression of miR-106a, thrombospondin 2 (THBS2), Bax, cleaved caspase-3 and Bcl-2, cell viability, relative caspase-3 activity and TNF-α, IL-1ß, IL-6 content were respectively detected by quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, Cell Counting Kit-8 (CCK-8) and enzyme linked immunosorbent assay (ELISA). The relationship between miR-106a and THBS2 was confirmed by dual luciferase reporter assay. RESULTS: MiR-106a was up-regulated in serum of sepsis patients, CLP-induced mice models and LPS-induced TCMK-1 cells. LPS reduced cell viability and Bcl-2 expression, and increased caspase-3 activity, Bax expression, the content of TNF-α, IL-1ß, IL-6. THBS2 was a target of miR-106a. The decreases of caspase-3 activity, TNF-α, IL-1ß, IL-6, Bax expression and the increases of cell viability, Bcl-2 expression caused by miR-106a knockdown were reversed when THBS2 silencing in LPS-stimulated TCMK-1 cells. CONCLUSION: MiR-106a aggravated LPS-induced inflammation and apoptosis of TCMK-1 cells via regulating THBS2 expression.

MiR-106a aggravates sepsis-induced acute kidney injury by targeting THBS2 in mice model

Abstract Purpose To investigate the role and related mechanisms of miR-106a in sepsis-induced AKI. Methods Serum from sepsis and healthy patients was collected, sepsis mouse model was established by cecal ligation and puncture (CLP). TCMK-1 cells were treated with lipopolysaccharide (LPS) and transfected with THBS2-small interfering RNA (siTHBS2), miR-106a inhibitor, miR-106a mimics and their negative controls (NCs). The expression of miR-106a, thrombospondin 2 (THBS2), Bax, cleaved caspase-3 and Bcl-2, cell viability, relative caspase-3 activity and TNF-α, IL-1β, IL-6 content were respectively detected by quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, Cell Counting Kit-8 (CCK-8) and enzyme linked immunosorbent assay (ELISA). The relationship between miR-106a and THBS2 was confirmed by dual luciferase reporter assay. Results MiR-106a was up-regulated in serum of sepsis patients, CLP-induced mice models and LPS-induced TCMK-1 cells. LPS reduced cell viability and Bcl-2 expression, and increased caspase-3 activity, Bax expression, the content of TNF-α, IL-1β, IL-6. THBS2 was a target of miR-106a. The decreases of caspase-3 activity, TNF-α, IL-1β, IL-6, Bax expression and the increases of cell viability, Bcl-2 expression caused by miR-106a knockdown were reversed when THBS2 silencing in LPS-stimulated TCMK-1 cells. Conclusion MiR-106a aggravated LPS-induced inflammation and apoptosis of TCMK-1 cells via regulating THBS2 expression.