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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.
Sepsis-induced acute kidney injury (AKI) is one of the most common causes of AKI, and elucidating its pathophysiology is crucial for preventing progression to chronic kidney disease (CKD) and avoiding dialysis. During septic AKI, increased sympathetic nerve activity is suggested due to hypotension, and adrenergic agonists are frequently administered to maintain hemodynamic stability. However, the role of renal sympathetic nerve signaling in AKI remains unclear. This study aimed to investigate the effects of renal sympathetic activation on septic AKI and to elucidate its intracellular mechanisms.
To achieve specific activation of renal sympathetic nerves, we established an optogenetic stimulation method. Optogenetics enables precise control of neuronal activity using light. We used genetically modified mice expressing channelrhodopsin (ChR2), a blue light–responsive cation channel, in sympathetic neurons (DbHCre―ChR2 mice). Bilateral renal sympathetic nerves were stimulated with blue LED light (20 Hz, 5 min). Lipopolysaccharide (LPS) was administered intraperitoneally, and renal function was evaluated 24 h later. This approach allows selective and noninvasive stimulation of renal sympathetic nerves, in contrast to conventional electrical stimulation.
Renal sympathetic stimulation significantly decreased plasma creatinine and BUN levels compared with non-stimulated controls. The expression of tubular injury markers (NGAL, KIM-1) was reduced, and histological assessment revealed attenuated tubular damage, suggesting a protective role of renal sympathetic signaling on renal tubules. Immunostaining for tyrosine hydroxylase (TH) demonstrated sympathetic fibers surrounding renal tubules. Among adrenergic receptor subtypes (α₁, α₂, β₁, β₂, β₃), β₂-adrenergic receptors were specifically expressed on tubular epithelial cells. Administration of the β₂-adrenergic receptor agonist salbutamol also conferred renal protection against LPS-induced AKI. In contrast, tubular β₂-adrenergic receptor knockout mice (SGLT2-Cre-ADRB2flox) exhibited aggravated tubular injury, indicating that renal sympathetic signaling exerts its renoprotective effect via β₂-adrenergic receptors on tubules.In in vitro experiments using human proximal tubular cells (HK-2), salbutamol reduced LPS-induced injury in a dose-dependent manner. RNA sequencing revealed that β₂-agonist treatment upregulated Metallothionein 1 (MT1), a zinc-regulatory and antioxidative gene. Gene ontology analysis confirmed enrichment of zinc-related pathways. Overexpression of MT1 in HK-2 cells suppressed LPS-induced injury, and upstream analysis identified induction of the zinc transporter ZIP10 (SLC39A10) by β₂-agonist stimulation.
Renal sympathetic activation protects against septic AKI by stimulating β₂-adrenergic receptors on tubular cells, leading to induction of the zinc-regulatory gene Metallothionein 1. This neuro–zinc–tubule axis represents a novel mechanism linking renal sympathetic signaling to tubular protection.
