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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.
Acute kidney injury (AKI) not only leads to the progression of chronic kidney disease and end-stage renal failure but also increases the risk of cardiovascular diseases and mortality. Cisplatin is a major tumoricidal drug used for a number of cancers. About 30% of patients treated with cisplatin develop AKI, which leads to the cessation of therapy. However, there is no definitive treatment for cisplatin-induced AKI, and the development of new preventive and therapeutic approaches is needed. Recently, the cholinergic anti-inflammatory pathway has attracted attention for its anti-inflammatory and renoprotective effects. The pathway mediated by macrophages has become clear, but the pathway that acts directly on the kidneys is not well understood. This study aims to clarify the renoprotective effects on cisplatin-induced AKI via parasympathetic nerve stimulation directly on the kidneys.
We administered nicotine (acetylcholine receptor agonist) to a mouse cisplatin induced AKI model, and evaluated plasma creatinine, tubular injury markers, inflammatory cytokine expression, and pathological findings. In vitro, we administered cisplatin and GTS-21 (selective α7 nicotinic acetylcholine receptor agonist) to HK-2 (human proximal tubular epithelial cell line) cells, and evaluated the expression of tubular injury markers and inflammatory cytokines. To elucidate the mechanism by which GTS-21 exerts renoprotection, the nuclear translocation of nuclear factor-κB (NF-κB) was assessed using immunostaining.
Administering nicotine to a mouse cisplatin-induced AKI model resulted in decreased plasma creatinine, reduced expression of tubular injury markers and inflammatory cytokines, and attenuation of tubular damage. Administration of cisplatin and GTS-21 to HK-2 cells reduced the expression of tubular injury markers and inflammatory cytokines. The nuclear translocation of NF-κB, which was increased by cisplatin administration, was suppressed by GTS-21.
The results indicated that parasympathetic nerve stimulation directly on the kidneys provided renoprotective effects against cisplatin-induced AKI. It was suggested that parasympathetic nerve stimulation inhibited the activation of NF-κB pathway and provided an anti-inflammatory effect. We need further investigations to elucidate the mechanisms, which leads to the development of new treatments.
