To study on the effect of sCD89–IgA on glomerular vascular endothelial cell proliferation in children with IgAVN, and to explore the mechanism by which sCD89–IgA is involved in the pathogenesis of pediatric IgAVN. The in vivo study used plasma and renal tissues from children diagnosed with IgAVN who were admitted to our department between May 2023 and June 2024. ELISA was used to detect the plasma concentration of sCD89–IgA, and the correlation between sCD89–IgA levels and urinary protein excretion was further analyzed. Renal tissue samples were classified into E0 and E1 subtypes; fluorescence co-localization was employed to assess the deposition of sCD89–IgA in glomeruli, while immunohistochemistry was used to evaluate the infiltration of CD68+ macrophages. As for in vitro cell experiments, HUVECs were treated with sCD89–IgA, and cell proliferation was detected by the CCK-8 assay. In addition, THP-1 cells were induced to differentiate into macrophages, which were then treated with sCD89–IgA followed by transcriptome analysis. Moreover, macrophages were treated with sCD89–IgA in the presence or absence of an IgA Fc fragment receptor blocker, and ELISA was used to quantify the intracellular levels of TNF-α and IL-1β. The 24-h urine protein level in children with IgAVN increased concomitantly with elevated plasma sCD89–IgA concentrations, showing a strong positive correlation between the two parameters (r = 0.8049, p < 0.0001). sCD89–IgA deposition and CD68+ macrophage infiltration were higher in E1-type than in E0-type IgAVN; however, sCD89–IgA did not significantly increase HUVEC proliferation. sCD89–IgA drives pro-inflammatory macrophage activation via the IgA-FcαRI pathway, as shown by transcriptome and blockade data. sCD89–IgA may mediate glomerular vascular endothelial cell proliferation through macrophage activation, thereby influencing urinary protein levels in children with IgAVN.
Yu et al. (Fri,) studied this question.