Factors affecting continuous renal replacement therapy duration in critically ill patients: A retrospective study.

INTRODUCTION: This study aimed to analyze the factors affecting continuous renal replacement therapy (CRRT) duration in critically ill patients and provide a reference for clinical treatment. MATERIAL AND METHODS: We divided patients into regional citrate anti-coagulation (RCA) and low-molecular-weight-heparin (LMWH) groups according to the anti-coagulation method and collected the relevant data, to analyze the factors associated with CRRT time. RESULTS: Compared with the LMWH group, the RCA group had a longer mean treatment time (55.36 ± 22.57 vs. 37.65 ± 27.09 h, p < 0.001), lower transmembrane pressure, and lower filter pressure, regardless of vascular access site. Multivariable linear regression analysis showed a significant correlation between anti-coagulation patterns, filter pressure at CRRT discontinuation, nurses' level of intensive care unit experience, pre-machine fibrinogen level, and CRRT time. CONCLUSION: Anti-coagulation is the most important factor affecting CRRT duration. Filter pressure, nurses' level of intensive care unit experience, and fibrinogen level also affecting CRRT duration.

MiR-501-5p alleviates cardiac dysfunction in septic patients through targeting NR4A3 to prevent its binding with Bcl-2.

Sepsis-induced myocardial dysfunction is a common complication in septic patients. To date, a limited number of biomarkers that could predict cardiomyocyte apoptosis have been explored. In this study, we successfully established a cecal ligation and puncture (CLP)-induced septic model, and it was found that miR-501-5p expression was down-regulated in peripheral blood samples of septic patients with cardiac dysfunction, lipopolysaccharide (LPS)-induced cardiomyocytes, and the myocardium and peripheral blood in the septic model. Moreover, it was revealed that miR-501-5p overexpression could increase left ventricular diastolic pressure (LVDP), fractional shortening (FS), ejection fraction (EF), and maximum rate of the rise of left ventricular pressure (+dp/dt) in vivo, while it decreased the levels of myocardial injury-related indicators. In addition, LPS induction accelerated apoptosis and elevated the inflammation in HL-1 and HCM cells, which could be reversed by miR-501-5p overexpression. Mechanistically, we considered nuclear receptor subfamily 4 group A member 3 (NR4A3) as the target of miR-501-5p, and it was found that miR-501-5p prevented the binding between NR4A3 and Bcl-2. It was found that miR-501-5p exerted an inhibitory effect on cardiomyocyte apoptosis and inflammation in a NR4A3-dependent manner. Overall, our results may provide evidence for consideration of miR-501-5p in the therapy of sepsis.