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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.
Nephrotic Syndrome is characterized by severe proteinuria and podocyte injury. Endothelial involvement is also common, but its significance is unknown. Here we investigated the role of CD93, a protein primarily expressed in endothelium, as a predictive biomarker and contributory etiologic factor of podocyte injury.
We studied 610 patients with different kidney disorders associated with nephrotic syndrome (idiopathic nephrotic syndrome [INS], membranous nephropathy, diabetic kidney disease, lupus nephritis, genetic nephrotic syndrome). CD93 was analyzed in urine and serum (ELISA), and/or kidney tissue (transcriptomic analysis and immunofluorescence). In a longitudinal cohort of patients with INS (n=298), we investigated the relationship between soluble CD93 and clinical outcomes. We performed several in vitro techniques to investigate the impact of soluble CD93 on the functionality of human podocytes and cellular source. Additionally, we tested efficacy of CD93 blocking antibody in 2 models of proteinuria (podocyte-specific TGFb1 [TGFb1]and Adriamycin[ADR]). We also use a CD93 global knockout (KO) mouse model to test the role of CD93 in the glomerular filtration barrier.
Soluble CD93 levels were high in urine and sera from ~90% patients with nephrotic syndrome, irrespective of the etiology. Remarkably, levels remained high in ~50% patients without proteinuria. In INS, high urinary CD93 levels associated with faster decline in kidney function, slower response to immunosuppression, and higher risk to develop proteinuria. In these patients, CD93 was highly expressed in the glomerular endothelium. Patients’ sera stimulated cultured human glomerular endothelial cells (GEnC), but not monocytes or other human vein umbilical endothelial cells, to release CD93. Soluble CD93 mediated podocyte injury via β1 integrin signaling. Using glom-on-a-chip, patients’ sera caused podocyte injury and increased albumin permeability; and these effects were mitigated by a CD93 antibody. In the TGFb1 and ADR mice, administration of CD93 blocking antibody mitigated proteinuria, podocyte loss and foot process effacement, and glomerulosclerosis. CD93 KO mice had normal podocyte count and morphology and albuminuria at baseline and were protected from ADR-podocyte injury.
Endothelial-released CD93 is a candidate predictive and therapeutic target in NS.
