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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.
Chronic kidney disease (CKD) affects nearly 700 million people worldwide, ranking among the top 10 causes of global mortality, while acute kidney injury (AKI) contributes to an additional 13 million cases annually, with over 1.7 million deaths, disproportionately in low- and middle-income countries [WHO, GBD 2020]. Traditionally, the kidney has been viewed as a peripherally regulated organ under sympathetic and parasympathetic control. However, advances in neuroscience highlight the phenomenon of neuroplasticity—the brain’s ability to reorganize neural networks in response to injury. This raises a provocative hypothesis: could the brain dynamically rewire its influence over renal function, thereby modulating CKD progression or AKI recovery?
I conducted a narrative review integrating literature from neuroscience, nephrology, autonomic physiology, and neuro-immune interactions. Data were sourced from PubMed, WHO reports, and recent reviews in Nature Reviews Nephrology, Kidney International, and The Lancet. The synthesis focused on:
1. Evidence of central neural remodeling in chronic stress and hypertension models.
2. Plasticity of brain circuits regulating renal sympathetic nerve activity.
3. Crosstalk between the brain, kidney, and immune system in CKD progression.
4. Emerging neuromodulation therapies such as vagus nerve stimulation (VNS), transcranial magnetic stimulation (TMS), and deep brain stimulation (DBS) as potential interventions for renal protection.
Preclinical and translational studies demonstrate that renal injury induces adaptive and maladaptive neuroplastic changes in central autonomic circuits. These alterations can exacerbate hypertension, inflammation, and fibrosis, yet may also reveal mechanisms for protective rewiring. Experimental models show that brain-driven modulation of renal sympathetic outflow influences glomerular hemodynamics and immune activation. Clinical studies further document structural brain changes in CKD patients, including cortical thinning and disrupted white matter connectivity, linked to uremic neurotoxicity and microvascular injury. Moreover, the kidney–gut–brain axis has emerged as a critical mediator of systemic inflammation and cognitive decline in dialysis populations. Collectively, these findings support a dynamic bidirectional brain–kidney dialogue with potential therapeutic leverage points.
I propose that the diseased kidney is not merely a passive target of neural input but an active partner in a neuroplastic brain–kidney loop. Harnessing neuroplasticity to promote adaptive rewiring may represent a transformative frontier in “Neuro-Nephrology.” Targeting the brain through non-invasive neuromodulation could complement conventional nephrology therapies, reduce global CKD and AKI burden, and provide equitable solutions for populations in resource-limited settings. This paradigm reframes kidney disease not only as a renal disorder but as a systemic neuro-immunological condition, opening novel avenues for precision medicine.
