Expression and mechanism exploration of miR-483-5p in children with IgA vasculitis with nephritis

IgA vasculitis with nephritis (IgAVN) represents the most serious renal complication in pediatric patients with IgA vasculitis (IgAV). To characterize miR‑483‑5p expression in pediatric IgAVN patients, evaluate its potential as a diagnostic biomarker, and elucidate underlying molecular mechanisms. A total of 150 children with IgAV (55 with IgAVN, 95 with non‑IgAVN) and 60 age‑ and gender‑matched healthy controls were enrolled in this retrospective clinical study. RT-qPCR was used to detect miR-483-5p and HDAC4 mRNA expression. ROC curve analysis was conducted to assess its tentative auxiliary screening capacity for IgAV-associated renal injury. Pearson correlation analysis was used to analyze the correlation between miR-483-5p expression and clinical indicators. Logistic regression analysis was used to identify factors independently associated IgAVN. Human glomerular mesangial cells (HGMCs) were treated with lipopolysaccharide (LPS) to construct cell model. miR-483-5p was markedly downregulated in the serum and renal tissues of children with IgAVN, and serum miR-483-5p exhibited significant discriminative capacity to distinguish children with concurrent IgAVN from IgAV patients without renal involvement in this retrospective cohort. MiR-483-5p expression was negatively correlated with renal function indicators, serum IgA and inflammatory factors, and its low expression was an independently associated factor for IgAVN. In vitro, LPS downregulated miR-483-5p, promoted HGMC proliferation and inflammatory response. MiR-483-5p directly targeted and negatively regulated HDAC4. Overexpression of miR-483-5p inhibited LPS-induced HGMC proliferation and inflammatory factor secretion, while HDAC4 overexpression reversed these effects. miR‑483‑5p is downregulated in children with IgAVN and may serve as a potential non‑invasive auxiliary indicator for pediatric IgAVN. miR‑483‑5p attenuates LPS‑induced HGMC proliferation and inflammation by targeting HDAC4 in vitro; however, the in vivo mechanistic relevance and clinical utility remain preliminary and require further validation.