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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.
Between late 2023 and early 2024, numerous cases of severe kidney dysfunction were reported in Japan among individuals who had taken beni-koji (red yeast rice) supplements contaminated with puberulic acid. Puberulic acid is a metabolite produced by certain Penicillium species. The information regarding the affected renal structures and underlying mechanisms remains limited. This study aimed to elucidate the localization of puberulic acid–induced inflammation in vivo and to assess its direct cytotoxic effects on cultured renal tubular cells.
Interleukin-6 (IL6) reporter mice (IL6-Luc) were intraperitoneally administered puberulic acid (5 mg/kg) or lipopolysaccharide (LPS) to visualize in vivo inflammatory responses using a bioluminescence imaging system. To evaluate tissue injury, C57BL/6 mice received intraperitoneal injections of puberulic acid (5 mg/kg), and kidney tissues were analyzed 2 days post-injection. Human proximal tubular epithelial cells (HK-2) were exposed to puberulic acid in vitro. Cell viability was assessed using the WST-8 assay, and protein expression was analyzed by Western blotting.
Results: In IL6-Luc mice, LPS induced a systemic inflammatory response throughout the body, whereas puberulic acid elicited a localized bioluminescent signal predominantly in the kidney region. In C57BL/6 mice, the administration of puberulic acid resulted in the expansion of the interstitial areas that were positive for transforming growth factor-β1 (TGFB1) and the macrophage markers CD68 and CD206. In vitro, HK-2 cells exposed to puberulic acid showed a concentration-dependent decline in viable cell numbers. The upregulation of mitochondrial injury markers was observed in Western blot analysis.
Puberulic acid specifically induces renal inflammation and exerts cytotoxic effects on proximal tubular epithelial cells through mitochondrial injury. These findings suggest that the kidney is a primary target organ for puberulic acid toxicity and that mitochondrial impairment may be a key mechanism underlying puberulic acid–induced nephropathy. Further studies are warranted to elucidate the molecular pathways involved and to evaluate the clinical relevance of puberulic acid exposure in humans.
