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IntroductionEarly identification of AKI was always considered to improve patients' prognosis. Some studies found that AKI early warning tools didn't affect patients' prognosis. Therefore, additional studies were necessary to explore the reasons.MethodsThis study was a secondary analysis of a multicenter randomized controlled trial that found electronic health record warnings for AKI did not influence patients' prognoses. Univariate, multivariate, subgroup, curve fitting, and threshold effect analysis were used to explore the association between AKI warnings detected by attending physicians and the patient's prognosis.ResultsA total of 6,030 AKI patients were included in the study. The patients were classified into two groups based on the rate of AKI alerts detected by attending physicians: the partial group (n = 5,377), and the complete group (n = 653). In comparison to the partial group, the complete group significantly decreased 14-day AKI progression, 14-day dialysis, and 14-day mortality, with adjusted ORs of 0.48 (0.33, 0.70), 0.26 (0.09, 0.77), and 0.53 (0.33, 0.84) respectively, and the complete group significantly improve the discharge to home, with an OR value of 1.50 (1.21, 1.87). When the rate of AKI alerts detected by the attending physicians as a continuity variable, we found that the rate of alerts seen by attending physicians was associated with 14-day mortality and the discharge to home, with adjusted ORs of 1.76 (1.11, 2.81) and 1.42 (1.13, 1.80). The sensitivity analysis, curve-fitting analysis, and threshold effect analysis also showed that the rate of alert seen by the attending physician was correlated with the patient's prognosis.ConclusionThe rate of AKI alert detection by attending physician were related to the patient's prognosis. The higher the rate of AKI alert detection by attending physicians, the better the prognosis of patients with AKI.

Background Acute kidney injury (AKI) is the most common cause of organ failure in multiple organ dysfunction syndrome (MODS) and is associated with increased mortality. This study aimed at determining the efficacy of sequential organ failure assessment (SOFA), and acute physiology and chronic health evaluation II (APACHE-II) scoring systems in assessing the prognosis of critically ill patients with AKI undergoing continuous renal replacement therapy (CRRT). At present, APACHE-II score and SOFA score were also used to evaluate and predict the prognosis of critically ill patients with AKI. Methods The predictive value of SOFA and APACHE-II scores for 28- and 90-d mortality in patients with AKI undergoing CRRT were determined by multivariate analysis, sensitivity analysis, and curve-fitting analysis. Results A total of 836 cases were included in this study. Multivariate Cox logistic regression analysis showed that SOFA scores were associated with 28- and 90-d mortality in patients with AKI undergoing CRRT. The adjusted HR of SOFA for 28-d mortality were 1.18 (1.14, 1.21), 1.24 (1.18, 1.31), and 1.19 (1.13, 1.24) in the three models, respectively, and the adjusted HR of SOFA for 90-d mortality was 1.12 (1.09, 1.16), 1.15 (1.10, 1.19), and 1.15 (1.10, 1.19), respectively. The subgroup analysis showed that the SOFA score was associated with 28-d and 90-d mortality in patients with AKI undergoing CRRT. APACHE-II score was not associated with 28- and 90-d mortality patients with AKI undergoing CRRT. Curve fitting analysis showed that SOFA scores increased had a higher prediction accuracy for 28- and 90-d than APACHE-II. Conclusions The SOFA score showed a higher accuracy of mortality prediction in critically ill patients with AKI undergoing CRRT than the APACHE-II score.

Background: Acute kidney injury (AKI) requiring continuous renal replacement therapy (CRRT) is a fatal and common clinical disorder in critically ill patients. Recent studies have shown that the relationship between BMI and the outcome of patients with AKI undergoing CRRT is conflicting. Methods: A retrospective cohort study based on data reuse. Univariate analysis, multi-factor regression analysis and subgroup analyses were used to explore the association of the BMI with the 28-days mortality risk in patients with AKI undergoing CRRT. Results: From January 2009 to September 2016, a total of 1120 cases met the inclusion criteria and were enrolled in this study. The univariate analysis showed that BMI was associated with 28-days mortality of patients with AKI undergoing CRRT, its HR value was 0.98 (0.96, 0.99). The multi-factor regression analysis showed that BMI was not associated with 28-days mortality of patients with AKI undergoing CRRT in the four models, the adjusted HR value of four models were 1.00 (0.96, 1.04), 1.01 (0.97, 1.04), 1.00 (0.96, 1.04) and 1.00 (0.96, 1.04), respectively. The subgroups analyses showed that the BMI was a risk factor of the 28-days mortality in patients with AKI undergoing CRRT when GFR ≥30 mL/min, its HR value was 1.04 (1.01, 1.09). Conclusion: Higher BMI was not a protective risk of 28-day mortality in patients with AKI undergoing CRRT. Especially, when GFR ≥30 mL/min, higher BMI increased the risk of the 28-day mortality rate in patients with AKI undergoing CRRT.

Objective To investigate the association between serum phosphate levels and the risk of 28-day mortality in critically-ill patients with septic acute kidney injury (AKI) undergoing continuous renal replacement therapy (CRRT). Methods This retrospective cohort study analysed data from critically-ill patients with septic AKI who underwent CRRT between January 2009 and September 2016. Demographic, clinical and routine biochemical data were retrieved from a database and analysed to identify risk factors for 28-day mortality. Results A total of 796 patients were included in the analyses. Multivariate regression analyses showed that phosphate (0 h), phosphate (24 h) and delta phosphate were associated with the 28-day mortality in patients with septic AKI undergoing CRRT. The adjusted odds ratios (95% confidence interval) were 1.12 (1.03, 1.22), 1.22 (1.14, 1.30) and 1.12 (1.04, 1.20) for phosphate (0 h), phosphate (24 h) and delta phosphate, respectively. Curve fitting and threshold analyses showed that when phosphate (0 h) was between 5.6 mg/dl and 8.7 mg/dl, phosphate (24 h) was >3.8 mg/dl and delta phosphate was >–1, the 28-day mortality risk increased significantly. Conclusion In patients with septic AKI undergoing CRRT, serum phosphate level was associated with the prognosis of patients in terms of 28-day mortality.

Objective To analyse the role of anticoagulation therapy in cardiopulmonary resuscitation (CPR) following an in-hospital cardiac arrest. Methods This single-centre retrospective cohort study enrolled patients treated with in-hospital CPR that met the inclusion and exclusion criteria. The patients were divided into a without anticoagulation group and an anticoagulation group. The main outcome measures were the restoration of spontaneous respiration, restoration of sinus rhythm (ROSR), restoration of spontaneous circulation (ROSC) and the hospital mortality. Results The study analysed 344 patients: 272 in the without anticoagulation group and 72 in the anticoagulation group. Multiple logistic regression analyses demonstrated that anticoagulation therapy improved ROSR (adjusted odds ratio [OR] 2.21, 95% confidence interval [CI] 1.23, 3.96) and ROSC (adjusted OR 1.91, 95% CI 1.08, 3.40), but it did not improve the restoration of spontaneous respiration (adjusted OR 1.64, 95% CI 0.72, 3.76) and hospital survival (adjusted OR 0.90, 95% CI 0.40, 1.99). Conclusion Anticoagulation therapy improved ROSR and ROSC, but did not decrease the mortality rate of hospitalized patients undergoing CPR following in-hospital cardiac arrest.

MicroRNAs can function as key tumor suppressors or oncogenes and act as biomarkers for cancer diagnosis or prognosis. Although high-throughput assays have revealed many miRNA biomarkers for pancreatic ductal adenocarcinoma (PDAC), only a few have been validated in independent populations or investigated for functional significance in PDAC pathogenesis. In this study, we correlated the expression of 36 potentially prognostic miRNAs within PDAC tissue with clinico-pathological features and survival in 151 Chinese patients. We then analyzed the functional roles and target genes of two miRNAs in PDAC development. We found that high expression of miR-186 and miR-326 predict poor and improved survival, respectively. miR-186 was over-expressed in PDAC patients compared with controls, especially in patients with large tumors (>2 cm), lymph node metastasis, or short-term survival (< 24 months). In contrast, miR-326 was down-regulated in patients compared with controls and displayed relatively increased expression in the patients with long-term survival or without venous invasion. Functional experiments revealed that PDAC cell proliferation and migration was decreased following inhibition and enhanced following over-expression of miR-186. In contrast, it was enhanced following inhibition and decreased after over-expression of miR-326. A luciferase assay indicated that miR-186 can bind directly to the 3'-UTR of NR5A2 to repress gene expression. These findings suggest that miR-186 over-expression contributes to the invasive potential of PDAC, likely via suppression of NR5A2, thereby leading to a poor prognosis; high miR-326 expression prolongs survival likely via the decreasing invasive potential of PDAC cells. These two miRNAs can be used as markers for clinical diagnosis and prognosis, and they represent therapeutic targets for PDAC.

Chronic pancreatitis is a progressive disease characterized by irreversible morphological changes to the pancreas, typically causing pain and permanent loss of function. It is a poorly understood disease with the pathogenesis remaining unclear. The authors' previous data demonstrated that the inhibition of Toll‑like receptor 4 (TLR4) using TLR4 antagonist kinase (TAK)‑242 attenuates taurocholate‑induced oxidative stress via the regulation of mitochondrial function in the pancreatic acinar cells of mice. In the present study, the effect of TAK‑242 on trinitrobenzene sulfonic acid (TNBS)‑induced chronic pancreatitis was investigated in rats. The results revealed that TAK‑242 attenuated the severity of chronic pancreatic injury, and regulated extracellular matrix secretion and cellular immunity. In addition, TAK‑242 treatment significantly decreased cell apoptosis, as evidenced by the reduction in Terminal deoxynucleotidyl transferase dUTP nick end labeling‑positive cells in pancreas tissue sections, and also promoted cell proliferation in TNBS‑treated animals. Furthermore, the results of the calibrated von Frey filament assay demonstrated that TAK‑242 could prevent the pancreatitis‑induced referred abdominal hypersensitivity. In summary, TAK‑242 exhibits protective effects against TNBS‑induced chronic pancreatitis and may be a potential therapeutic strategy for the treatment of patients with chronic pancreatitis. [ABSTRACT FROM AUTHOR]