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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.
Beni-Koji, a red mold rice supplement, has recently been implicated in acute kidney injury cases in Japan. Although the clinical and laboratory features of Beni-Koji-associated nephropathy have been increasingly characterized, the molecular and cellular mechanisms underlying renal injury remain poorly understood.
We performed spatial transcriptomic analysis using Visium HD on renal biopsy tissues from Japanese patients diagnosed with Beni-Koji supplement-induced kidney injury. Formalin-fixed, paraffin-embedded (FFPE) samples from confirmed cases were processed for high-resolution transcriptomic profiling. Data were analyzed with Seurat for clustering, cell type annotation, and identification of differentially expressed genes (DEGs) among injured and control regions.
Spatial transcriptomics revealed pronounced alterations in proximal tubular cells, including upregulation of stress response and apoptotic pathways (e.g., CASP3, JUN, DUSP1). Myofibroblast activation and endothelial cell injury signatures were detected in affected areas. Pathway enrichment analysis identified involvement of AP-1 signaling and complement activation in the pathogenesis. Injury-related Gene Ontology terms such as “response to oxidative stress” and “blood vessel development” were significantly enriched. Despite supplement cessation, most patients retained reduced eGFR, correlating with persistent tubular injury signatures.
This study provides the first spatial molecular map of Beni-Koji-associated human renal injury and underscores the utility of Visium HD-based transcriptomics for characterizing cellular heterogeneity and pathogenic mechanisms. Results highlight novel therapeutic targets and inform clinical management strategies for supplement-induced nephropathy.
