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Preparing your E-Poster
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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.
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Abstract titles should be brief and reflect the content of the abstract.
Peritoneal dialysis (PD) is a critical treatment for end-stage renal disease. Peritonitis, a common complication of PD, is a major cause of technical failure and peritoneal fibrosis. Evidence suggests that even after clinical cure, PD patients with a history of peritonitis still exhibit a significantly higher risk of progressive peritoneal fibrosis, but the underlying mechanism remains unclear. This study employs single-cell transcriptomics to investigate the key mechanisms of peritoneal fibrosis during the post-inflammatory peritoneal phase, aiming to identify novel therapeutic targets for clinical intervention.
We performed single-cell RNA sequencing (scRNA-seq) on peritoneal effluent cells from PD patients who underwent catheter placement at our center between 2019 and 2022. Based on clinical profiles, patients were stratified into two groups: the post-inflammatory peritoneal phase group (PS group, n=5) and the control group (CTL group, n=4). UMAP clustering, pseudotime trajectory analysis, and functional enrichment were applied to delineate gene expression changes and signaling pathways in mesothelial cells during the post-inflammatory phase.
1. Peritoneal effluent cells comprised nine distinct subsets: mesothelial cells (1.9%), T cells (47.7%), monocytes (17.0%), dendritic cells (13.8%), macrophages (8.4%), NK cells (5.1%), B cells (4.5%), neutrophils (0.2%), and fibroblasts (0.2%) (Figure 1A). Compared to the CTL group, the PS group exhibited reduced mesothelial cells (CTL: 0.9% vs. PS: 4.0%) and expanded monocytes (CTL: 10.0% vs. PS: 20.5%) and macrophages (CTL: 3.3% vs. PS: 10.9%) (Figure 1B).
2. Clustering of mesothelial cells identified a dominant subset (Cluster 0) enriched in the PS group (Figure 1C). GO analysis highlighted its association with extracellular matrix organization, collagen fibril assembly, and angiogenesis, while KEGG pathways implicated TGF-β signaling and ECM-receptor interactions—both hallmarks of fibrosis—suggesting this subset underwent epithelial-mesenchymal transition (EMT).
3. Pseudotime trajectory analysis resolved mesothelial cells into three states (S1–S3), with Cluster 0 primarily localizing to the terminal pro-fibrotic state (S3). Differential gene expression in S3 confirmed upregulation of fibrosis-driving genes, indicating sustained pro-fibrotic reprogramming post-peritonitis.
4. Immune profiling revealed elevated monocyte-macrophage populations in the PS group (CTL: 13.4% vs. PS: 31.5%, *p* < 0.05). CellChat analysis uncovered active crosstalk between mesothelial cells and monocyte-macrophages via specific ligand-receptor pairs.
(A) UMAP (Uniform Manifold Approximation and Projection) plot visualizing clustering analysis of the PS and CTL groups.
(B) Cell types and their proportions in peritoneal dialysis effluent from the PS and CTL groups. The horizontal axis represents cell proportions, and the vertical axis represents group classification.
(C) UMAP plot visualizing the distribution of seven mesothelial cell subsets and their comparison between the PS and CTL groups.
This study pioneers the discovery that mesothelial cells retain pro-fibrotic EMT features during the post-inflammatory peritoneal phase, despite clinical resolution of peritonitis. Our findings unravel the mechanistic basis for persistent fibrosis and propose targeting EMT regulators as a therapeutic strategy, with direct implications for improving PD outcomes.
This abstract was previously presented at the APCM-ISPD conference. Re-publication of the abstract here is permitted with authorization from the original copyright holders (the conference organizers).
