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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.
Leptospirosis, a neglected zoonotic disease caused by Leptospira infection, is increasingly recognized as a contributor to both acute and chronic kidney disease. However, studies on the pathophysiology of leptospirosis kidney disease remain limited. To elucidate the underlying mechanisms of the transition from acute to chronic kidney disease due to Leptospira infection, we performed single-nucleus RNA sequencing and spatial transcriptomics on kidney tissues from infected mice.
1. Mouse model for leptospiral kidney disease
2. High-dimensional flow cytometry for analyzed leukocyte subpopulations in peripheral blood at early infection stages
3. Single-nucleus RNA sequencing for profiling changes in kidney cell populations
4. Spatial transcriptomics for mapping of the spatial distribution and transcriptional profiling
The study investigated the pathogenic mechanisms underlying the transition from acute to chronic phases during leptospirosis kidney disease progression using a murine model. Infected mice exhibited renal injury and bacterial adherence to the renal tubules by day 28 post-infection. Renal pathology revealed tubular degeneration, inflammation, and fibrosis characteristic of chronic kidney disease. Single-nucleus RNA sequencing revealed 33 transcriptionally distinct renal cell clusters, including various renal cell types. Normal proximal tubular cells decreased on the 7th day post-infection, with an increment of injured proximal tubular cells. Initially, fibroblast numbers increased in the infected group, suggesting early fibrosis development. By day 28, immune cell populations grew, implicating their involvement in chronic renal pathology. Systemic immune responses were further assessed by high-dimensional flow cytometry of peripheral blood at early and late infection stages. Notable alterations in CD4+ T cell subsets, including increases in Th17 and regulatory T cells during early infection, as well as an expansion of CD11b+Gr-1+ myeloid-derived suppressor cell-like populations, suggesting the activation of immunosuppressive mechanisms that may facilitate persistent infection and chronic inflammation. Spatial transcriptomics of formalin-fixed, paraffin-embedded kidney sections from infected mice was performed using the 10X Genomics Visium CytAssist platform. This approach enabled comprehensive mapping of the spatial distribution and transcriptional profiling of injured proximal tubules and infiltrating immune cells. The spatial landscape revealed a profibrotic and inflammatory microenvironment involving interactions among injured tubules, fibroblasts, immune cells, and endothelial cells, which may contribute to the transition from acute kidney injury to chronic kidney disease.
This study provides novel spatial and transcriptional insights into the dynamic interplay between tubular injury, immune responses, and fibrosis in leptospirosis kidney diseases. These findings potential therapeutic targets to slow or prevent chronic kidney injury induced by Leptospira infection. (This abstract was also submitted for the APCN x TSN 2025 congress. By submitting the abstract to WCN'26, abstract authors declare that re-submitting the abstract is permitted by the organizers of the previous meeting)
