Background: Diagnosing acute kidney injury (AKI) stage 3 in critically ill patients may help physicians in making treatment decisions. This diagnosis relies chiefly on urinary output and serum creatinine, which may be of limited value. This study aimed to explore the diagnostic performance of renal resistive index (RRI) and semiquantitative power Doppler ultrasound (PDU) scores in predicting AKI stage 3 in patients with sepsis or cardiac failure. Methods: This study is a prospective observational study that included 83 patients (40 with sepsis and 43 with cardiac failure). Renal resistive index and semiquantitative PDU scores were measured within 6 hours following admission to the intensive care unit. Acute kidney injury was defined according to the criteria set by Kidney Disease Improving Global Outcomes. Results: The predictive values of RRI (area under the curve [AUC] = 0.772, 95% confidence interval [CI] = 0.658-0.886) and PDU score (AUC = 0.780, 95% CI = 0.667-0.892) were similar in all patients. Power Doppler ultrasound score (AUC = 0.910, 95% CI = 0.815-1.000) could effectively predict AKI stage 3 in the cardiac failure subgroup, and the optimal cutoff for this parameter was ≤ 1 (sensitivity = 87.5%, specificity = 92.6%, Youden index = 0.801, accuracy in our population = 90.7%). However, PDU scores (AUC = 0.620, 95% CI = 0.425-0.814) could not predict AKI stage 3 in the sepsis subgroup. The predictive values of RRI for AKI stage 3 in the cardiac failure (AUC = 0.820, 95% CI = 0.666-0.974) and sepsis (AUC = 0.724, 95% CI = 0.538-0.910) subgroups were similar. Conclusions: Power Doppler ultrasound scores could effectively predict AKI stage 3 in patients with cardiac failure but not in patients with sepsis. Renal resistive index is a poor predictor of AKI stage 3 in patients with sepsis or cardiac failure.
Background: Severity index and plasma paraquat (PQ) concentration can predict the prognosis of patients with PQ poisoning. However, the better parameter is yet to be systematically investigated and determined. Thus, we conduct this systematic review and meta-analysis to investigate the prognostic value of severity index and plasma PQ concentration in patients with PQ poisoning. Methods: We searched PubMed, Embase, Web of Science, ScienceDirect, and Cochrane Library to identify all relevant papers that were published up to March 2019. All diagnostic studies that compared severity index and plasma PQ concentration to predict mortality in patients with PQ poisoning were enrolled in this meta-analysis. Odds ratios (ORs) with 95% confidence intervals (CIs) for individual trials were pooled using a random-effect model. We also aggregated heterogeneity testing, sensitivity analysis, and publication bias analysis. Results: Ultimately, seven studies involving 821 patients were included. The pooled OR with a 95% CI of severity index was 24.12 (95% CI: 9.34–62.34, P < .001), with an area under the curve of 0.88 (95% CI: 0.85–0.90), sensitivity of 0.84 (95% CI: 0.74–0.91), and specificity of 0.81 (95% CI: 0.75–0.87). Meanwhile, the pooled OR with 95% CI of plasma PQ concentration was 34.39 (95% CI: 14.69–80.56, P < .001), with an area under the curve of 0.94 (95% CI: 0.91–0.96), sensitivity of 0.86 (95% CI: 0.75–0.93), and specificity of 0.89 (95% CI: 0.76–0.95). Sensitivity analysis demonstrated the stability of the results of our meta-analysis. No significant publication bias was observed in this meta-analysis. Conclusion : Overall, this study indicated that severity index and plasma PQ concentration have relatively high-prognostic value in patients with PQ poisoning, and that the sensitivity and specificity of plasma PQ concentration are superior to those of severity index.
In recent years, the incidence and mortality of myocardial infarction (MI) have been increasing throughout the world, threatening public health. Non-coding RNAs (ncRNAs), including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), play critical roles in the progression of MI. The present study aimed to investigate the role of lncRNA AK006774 in the progression of myocardial infarction and find out novel therapeutic or diagnostic target of myocardial infarction. A mouse ischemia/reperfusion (I/R) model and 2,3,5-Triphenyte-trazoliumchloride (TTC) staining were performed to evaluate the effects of AK006774 on I/R injury in vivo. Hypoxia/reoxygenation (H/R) models using primary cardiomyocytes have been established. Flow cytometry and Terminal Deoxynucleotide Transferase dUTP Nick End Labeling (TUNEL) assays were performed to evaluate the effects of AK006774 on cardiomyocyte apoptosis. Luciferase and RNA pull-down assays were performed to verify the interaction between miR-448 and its targets. Western blotting and quantitative PCR were performed to determine protein and gene expression, respectively. We first found that AK006774 overexpression reduced I/R-induced infarct area and cardiomyocyte apoptosis in vivo. Accordingly, AK006774 inhibited apoptosis and oxidative stress in cardiomyocytes subjected to H/R treatment in vitro. Mechanistically, AK006774 modulated the expression of bcl-2 by sponging miR-448. Overexpression of miR-448 antagonized the effects of AK006774 on cardiomyocyte apoptosis. The AK006774/miR-448/bcl-2 signaling axis acts as a key regulator of I/R injury and may be a potential therapeutic or diagnostic target for the treatment of MI.
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