Purpose: Exploring the risk factors for mortality of hemodialysis patients undergoing COVID-19 and the changes in mortality before and after the opening of the epidemic in northern Hunan province, China.
Methods: We analyzed 230 hemodialysis patients with COVID-19 in the Yiyang Central Hospital from November 01, 2022 to February 28, 2023. Demographic data, laboratory data and public diseases were collected.
Vascular calcification is considered to be a killer of the cardiovascular system, involved inflammation and immunity. There is no approved therapeutic strategy for the prevention of vascular calcification. Sinomenine exhibited anti-inflammatory and immunosuppressive effects.
View Article and Find Full Text PDFBackground: Recent clinical evidences show that caspase-1 inhibitor-VX-765 attenuates atherosclerosis in ApoE deficient mice. However, there is rarely information about the effect of VX-765 on hyperphosphatemia-induced vascular smooth muscle cells (VSMCs) calcification or vascular calcification in chronic kidney disease (CKD) rats. Here we investigate the effect of VX-765 on vascular calcification in uremia circumstances.
View Article and Find Full Text PDFBackground: Reduced left ventricular ejection function (LVEF) was associated with increased mortality in patients with peritoneal dialysis (PD) in Asia and the United States of America. The neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) were correlated with LVEF in PD. However, little information is available regarding the relationship between monocyte-to-lymphocyte ratio (MLR), left ventricular ejection fraction (LVEF), and the use of NLR, PLR, and MLR in predicting left ventricular systolic dysfunction (LVSD) in patients with PD.
View Article and Find Full Text PDFBackground: Hyperphosphatemia (HP) is associated with vascular calcification (VC) in chronic kidney disease (CKD). However, relationship between HP-induced-endothelial extracellular vesicles (HP-EC-EVs) and VC is unclear, and miR expression in HP-EC-EVs has not been determined.
Methods: We isolated HP-EC-EVs from endothelial cells with HP and observed that HP-EC-EVs were up-taken by vascular smooth muscle cells (VSMCs).