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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.
Ketone bodies have long been considered alternative energy sources to glucose during fasting periods. However, their potential to protect organs has recently attracted more scholarly attention. This study aimed to evaluate the renoprotective effects of ketone bodies using a mouse model of adenine-induced nephropathy.
To assess the effects of exogenous ketone body supplementation, 1,3-butanediol—a precursor of β-hydroxybutyrate (BHB)—was given orally to mice with adenine-induced nephropathy. To explore the role of systemic and renal ketogenesis, adenine nephropathy was induced in mice with liver- or proximal tubule-specific deletion of 3-hydroxy-3-methylglutaryl-CoA synthase 2 (Hmgcs2), the key enzyme in ketogenesis. Additionally, to determine if the renoprotective effects of 1,3-butanediol depend on increased ATP production, we created proximal tubule-specific knockout mice lacking succinyl-CoA:3-ketoacid CoA transferase (Scot). Scot is an essential enzyme required for ketone body utilization.
In the adenine nephropathy model, oral administration of 1,3-butanediol reduced plasma cystatin C levels and histological damage. These effects were associated with reduced cell death, as indicated by TUNEL staining, along with decreased expression levels of genes related to inflammation, fibrosis, and apoptosis. Conversely, deficiency of Hmgcs2 specifically in the liver or proximal tubules did not exacerbate the elevation of plasma cystatin C levels in adenine-induced kidney injury. Although 1,3-butanediol significantly increased renal Hmgcs2 expression, its kidney-protecting effects remained even in mice lacking Hmgcs2 specifically in proximal tubules. On the other hand, deficiency of Scot in proximal tubules negated the protective impact of 1,3-butanediol in adenine nephropathy.
Exogenous ketone body supplementation protects the kidneys through Scot-mediated ketolysis in the adenine nephropathy model. In contrast, endogenous ketogenesis limited to the systemic or kidney-specific level alone was not enough to provide kidney protection. These findings indicate that systemic administration of ketone bodies and the subsequent enhancement of renal Scot-mediated ketolysis could be a promising treatment for chronic kidney disease.
