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Kidney Week

Abstract: TH-PO0131

Self-Powered Hybrid Nanogenerator-Driven Vagus Nerve Stimulation System Attenuates AKI and Its Transition to CKD

Session Information

  • AKI: Mechanisms - 1
    November 06, 2025 | Location: Exhibit Hall, Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Jin, Meiling, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing, China
  • Li, Diangeng, Capital Medical University Beijing Ditan Hospital, Beijing, China
  • Sun, QianMei, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing, China
Background

Acute kidney injury (AKI) is a common clinical syndrome that can progress to chronic kidney disease (CKD), yet effective therapeutic approaches remain limited. Vagus nerve stimulation (VNS) has demonstrated therapeutic potential by modulating autonomic nervous and immune responses, but conventional VNS systems rely on external power sources, limiting their clinical applicability. This study developed a self-powered VNS system based on hybrid nanogenerators (H-NG) for treating AKI and AKI-to-CKD transition.

Methods

An AKI-CKD mouse model was established through ischemia-reperfusion (I/R) injury combined with contralateral nephrectomy. The mice received H-NG-driven low-level VNS (LL-VNS, 10 μA, 2 Hz, 30 min) intervention. Evaluations included renal function (serum creatinine, BUN), renal pathology (PAS/Masson staining), gut microbiota (metagenomic sequencing), serum metabolome (LC-MS), and renal proteome (DIA) analysis.

Results

LL-VNS significantly reduced serum creatinine levels in the AKI-CKD model and alleviated tubular necrosis and fibrosis. Metagenomic analysis revealed that LL-VNS upregulated beneficial bacteria (e.g., Lachnospiraceae) while downregulating pro-inflammatory bacteria (e.g., Bacteroidales). Metabolomics identified restored levels of key metabolites (e.g., arachidonic acid, 5-aminolevulinic acid), and proteomics suggested that LL-VNS inhibits fibrosis through the gut-kidney axis by modulating renal signaling pathways such as AKT3-PI3K.

Conclusion

The self-powered LL-VNS system safely and effectively mitigates AKI progression to CKD, with mechanisms involving gut microbiota modulation and metabolic-protein network restoration, providing a novel neuromodulation strategy for kidney diseases.

Digital Object Identifier (DOI)