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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.
Systemic lupus erythematosus (SLE) frequently involves the kidneys, leading to lupus nephritis (LN). The complex pathogenesis of LN, coupled with the lack of efficient in vitro models, severely hampers drug development and personalized therapeutic strategies. This study aimed to establish a novel LN research platform using kidney organoids to recapitulate LN pathological processes in a highly biomimetic in vitro setting, thereby facilitating the investigation of LN pathogenesis, high-throughput drug screening, and the development of personalized treatment approaches to advance precision medicine in LN.
Human induced pluripotent stem cells (hiPSCs) were directedly differentiated into 3D kidney organoids, establishing a highly biomimetic in vitro model containing glomerular and tubular structures. Plasma samples were collected from patients with mild-to-moderate and severe LN. Upon reaching maturity with developed nephron structures at day 21, kidney organoids were stimulated with LN patient plasma for 72 hours to construct in vitro LN models. Pathological changes induced by LN plasma in the organoids were investigated using histochemical staining, immunofluorescence, and transcriptome sequencing.
Compared to stimulation with plasma from healthy controls, LN patient plasma stimulation for 72 hours induced significant morphological alterations in kidney organoids, as demonstrated by H&E staining, electron microscopy, and immunofluorescence. The expression of the podocyte marker Synaptopodin was markedly decreased, accompanied by evident foot process effacement. Staining for the tubular marker Lotus Tetragonolobus Lectin (LTL) was significantly reduced, indicating tubular atrophy and luminal structural disintegration. Furthermore, the expression of the tubular injury marker KIM-1 and the fibrosis marker Fibronectin 1 (FN1) was significantly upregulated. Transcriptome sequencing analysis revealed that stimulation with plasma from severe LN patients exerted a more pronounced impact on the organoid transcriptome compared to plasma from mild-to-moderate cases. Specific genes and pathways were uniquely enriched in organoids treated with plasma from severe LN patients.
This study successfully established a novel kidney organoid-based platform for LN research. This platform not only provides a powerful tool for elucidating LN mechanisms but also offers a new avenue for drug screening and personalized therapy. It demonstrates substantial innovation and translational potential, with future applications extendable to the study of other hereditary or acquired kidney diseases, thereby promoting the advancement of precision medicine in nephrology.
