These findings demonstrate that FGF23 levels are significantly higher in hemodialysis patients than that in peritoneal dialysis patients. We demonstrate an important association between dialysis modality (HD vs CAPD) and higher FGF23, independent of classical determinants (serum calcium and phosphate level).

Purpose: To investigate the effect of miR-486 on rats with acute myocardial infarction (AMI), and its mechanism of action.Methods: A rat model of AMI was established. They were randomly divided into 4 groups, namely, sham, model, agomiR-486 and antagomiR-486 groups, respectively. Rats in these different groups were treated with agomiR-21 (5 μL, 40 nmol/mL), antagomiR-21 (5 μL, 40 nmol/mL) or agomiR-NC (5 μL, 40 nmol/mL), respectively. Then, key miRNAs were sorted out using gene-chip assay and verified by quantitative reverse transcription polymerase chain reaction (qRT-PCR) assay. Luciferase reporter gene assay was conducted to determine the interaction between miR-486 and gene of PTEN. After intraperitoneal injection of agomiR-486 and antagomiR-486, hemodynamics was measured to determine the effect of miR-486 on myocardial function of the rats. The effect of miR-486 expression level on the expression of myocardial enzymes in serum, the morphology of myocardial tissues, and the apoptosis of myocardial tissues in rats, were investigated. Additionally, the effect of miR-486 expression level on PTEN/AKT signaling pathway in the rats was determined by Western blotting.Results: The results of gene-chip and qRT-PCR assays revealed that there were 8 differentially expressed genes in rat myocardial tissues in the model group when compared with the sham group. MiR-486 improved the cardiac function of rats and the morphology of myocardial tissues, but reduced AMI-induced apoptosis of myocardial cells and the expression of myocardial enzymes (markers of myocardial injury) in a dose-dependent manner (p < 0.05). The results of luciferase reporter gene assay showed that PTEN was a direct target of miR-486. In rat models of AMI, a raised expression of miR-486 remarkably suppressed the protein expression level of PTEN and up-regulated that of p-AKT/AKT (p < 0.05).Conclusion: MiR-486 protects against AMI in rats probably by targeting PTEN and activating the AKT signaling pathway. The results of the current study may provide new insights for the treatment of AMI.

Aim: To investigate the prognosis of soluble ST2 (sST2), galectin-3 and N-terminal pro-B-type natriuretic peptide (NT-proBNP) for death related to ischemic and nonischemic etiology of acute heart failure (HF). Methods: The associations between biomarkers and death were determined in 1020 patients admitted to hospital with acute HF. Results: During 1-year follow-up, 162 patients died. Multivariable regression analysis showed that the hazard ratios of sST2 and NT-proBNP for 1-year all-cause death was similar and remained significant between ischemic and nonischemic HF patients. However, galectin-3 was not significantly associated with death when sST2 and NT-proBNP were incorporated into model in ischemic HF patients. Conclusion: There is no etiology dependent prognostic ability of NT-proBNP or ST2 in patients with acute HF, but for galectin-3 there is no added prognostic ability in ischemic HF.