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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Endothelial dysfunction is increasingly recognized in childhood idiopathic nephrotic syndrome (INS), but this remains an understudied field. We tested the hypothesis that silent inflammation is linked to endothelial dysfunction.
The study includes 128 children with INS and 34 healthy participants (n=22 adults, n=12 children). In serum, we measured levels of TNFR1 and TNFR2 (inflammation) and angiopoietin-2 (Ang-2) (endothelial activation) using an automated immunoassay system. In kidney tissue, we analyzed expression of the same targets using available RNAseq datasets. We performed in vitro studies to test the effect of INS sera on human glomerular endothelial cells (GEnC).
Serum TNFR1, TNFR2 and Ang-2 levels were higher in INS patients with new onset INS or in relapse compared to controls; and levels were above normal range in ~30% of patients in remission. There was a strong correlation between serum TNFR1 and TNFR2, and between these markers and Ang-2. Higher serum TNFR1 and TNFR2 levels, but not Ang-2, associated with higher proteinuria and hypoalbuminemia. TNFR1 and TNFR2 mRNA expression was increased in several kidney cells, including endothelium, in patients with INS. TNFR1 and TNFR2 mRNA expression in kidney endothelial cells positively correlated with Ang-2 mRNA levels. Serum from INS patients activated GEnC as noted by the increase in Ang-2 mRNA expression, release of Ang-2 from GEnC lysates, and increased glucocorticoid receptor expression. Dexamethasone prevented GEnC activation by INS sera.
Silent inflammation is linked to endothelial dysfunction in INS; and steroids directly mitigate GEnC activation in these patients.
