Parenting self-efficacy and parenting stress mediates the effects of the association of perceived social support and readiness for discharge among parents of children with primary nephrotic syndrome.

PURPOSE: To investigate the level of readiness for discharge among parents of children with primary nephrotic syndrome and to explore the mediating role of parenting self-efficacy and parenting stress between perceived social support and readiness for discharge. DESIGN AND METHODS: A cross-sectional study was conducted in five large tertiary general hospitals in Hunan, China. Data related to demographics, perceived social support, parenting self-efficacy, parenting stress, and readiness for discharge were collected from 350 parents of children diagnosed with primary nephrotic syndrome. Path analysis was used to determine the mediating roles of parenting self-efficacy and parenting stress in the relationship between perceived social support and readiness for discharge. RESULTS: Parents of children with nephrotic syndrome in China experienced low perceived social support, low readiness for discharge, and high parenting stress. Factors influencing readiness for discharge include the child's age, duration of illness, first episode or relapse, parental literacy and marital status. Parenting self-efficacy and parenting stress mediated the effects of the association of perceived social support and readiness for discharge. CONCLUSION: Perceived social support influences the readiness of parents of children with nephrotic syndrome. Parenting self-efficacy and parenting stress have a chain mediating effect of the association of perceived social support and readiness for discharge. PRACTICE IMPLICATIONS: This study emphasizes the mediating role of the psychological state of the child's parents. Nurses should take steps to increase perceived social support and parenting self-efficacy of the child's parents and to reduce parenting stress in order to improve readiness for discharge.

Astragaloside IV Inhibits Galactose-Deficient IgA1 Secretion via miR-98-5p in Pediatric IgA Nephropathy.

Purpose: The factor associated with IgA nephropathy (IgAN) is an abnormality of IgA known as galactose-deficient IgA1 (Gd-IgA1). The purpose of this study was to determine the molecular role played by miRNAs in the formation of Gd-IgA1 in IgAN and investigate the regulatory role of Astragaloside IV (AS-IV) in miRNAs. Patients and methods: Bioinformatics analysis, along with functional and mechanistic experiments, were used to investigate the relationship and function of miRNA, ß-1, 3-galactosyltransferase (C1GALT1), Gd-IgA1, and AS-IV. Analyses involved a series of tools, including quantitative real-time polymerase chain reaction (qRT-qPCR), Western blot, enzyme-linked immunosorbent assay (ELISA), Vicia Villosa lectin-binding assay (VVA), Cell counting kit-8 assay (CCK-8), and the dual-luciferase reporter assay. Results: miRNA screening and validation showed that miR-98-5p was significantly upregulated in the peripheral blood mononuclear cells (PBMCs) of pediatric patients with IgAN compared with patients diagnosed with mesangial proliferative glomerulonephritis (MsPGN) and immunoglobulin A vasculitis nephritis (IgAV-N), and healthy controls (p < 0.05). Experiments with the dual-luciferase reporter confirmed that miR-98-5p might target C1GALT1. The overexpression of miR-98-5p in DAKIKI cells decreased both the mRNA and protein levels of C1GALT1 and increased the levels of Gd-IgA1 levels; these effects were reversed by co-transfection with the C1GALT1 plasmid, and vice versa. In addition, AS-IV downregulated the levels of Gd-IgA1 level in DAKIKI cells by inhibiting miR-98-5p. Conclusions: Our results revealed that AS-IV could inhibit Gd-IgA1 secretion via miR-98-5p. Increased levels of miR-98-5p in pediatric IgAN patients might affect the glycosylation of IgA1 by targeting C1GALT1. In addition, our analyses suggest that the pathogenesis of IgAN may differ from that of IgAV-N. Collectively, these results provide significant insight into the pathogenesis of IgAN and identify a potential therapeutic target.