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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.
Idiopathic nephrotic syndrome (INS) is viewed as a podocyte-specific disease. Recent reports indicate endothelial involvement, but its significance is unclear. Here, we investigated the relationship between the glomerular expression of selected genes relevant to endothelial health and clinical markers of disease severity.
We analyzed publicly available RNA seq data from micro-dissected human glomeruli performed by the NEPTUNE consortium. Because our group previously showed evidence of endothelial glycocalyx injury and endothelial activation, this study focused on 10 genes highly relevant for endothelial homeostasis and barrier integrity (NOS3, ESAM, ESM1), endothelial glycocalyx remodeling (HPSE, HYAL1, MMP2, MMP9, ADAMTS1) and endothelial activation (ICAM1, CAV1). The population included 153 patients with INS (n=70 minimal change disease [MCD] and n=83 focal segmental glomerulosclerosis [FSGS]) from the NEPTUNE cohort study and 53 control participants. Validation studies, including animal and cell culture experiments, were performed. Relationship between gene expression and clinical features (kidney function, ultrastructural changes in podocytes and glomerular endothelium, interstitial fibrosis and tubular atrophy [IF/TA] was studied using one-way ANOVA and Tukey’s multiple comparisons test Pearson Correlation and Cohen’s d statistics.
Transcriptomic analysis revealed that all genes of interest were highly expressed in glomeruli from INS patients compared to controls, except for ESM1 and MMP9 which were decreased. Expression of endothelial-specific genes correlated with those of glycocalyx injury and cell activation. HPSE, ADAMTS1, ICAM1, and CAV1 expression was inversely associated with kidney function, whereas ADAMTS1 showed a positive association with proteinuria. NOS3, HPSE and ADAMTS1 associated with podocyte foot process effacement and ICAM1 with podocyte detachment. HPSE and MMP2 associated with ultrastructural endothelial injury, whereas HPSE, MMP2, ICAM1 and CAV1 associated with IF/TA. Several genes (ESM1, HPSE, HYAL1, MMP2, and ICAM1) were also dysregulated in experimental INS, and validated in cultured glomerular endothelial cells (NOS3 and heparanase) following exposure to INS sera.
INS involves dysregulation of genes relevant for endothelial health.
