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Abstract: SA-PO675

Intraperitoneal Pressure Induces Peritoneal Dialysis-Related Peritoneal Fibrosis and Stampede Phenomenon Through CD44 Signaling

Session Information

  • Home Dialysis - II
    November 04, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Dialysis

  • 802 Dialysis: Home Dialysis and Peritoneal Dialysis


  • Chen, Yu-Wei, Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
  • Chen, Cheng-hsien, Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
  • Wu, Mai-Szu, Taipei Medical University Shuang Ho Hospital Ministry of Health and Welfare, New Taipei City, Taiwan
  • Hsu, Yung-Ho, Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan

Peritoneal dialysis (PD) is a widely used sustainable kidney replacement therapy. Prolonged use of peritoneal dialysis fluids is associated with mesothelial-mesenchymal transition, peritoneal fibrosis, and eventual ultrafiltration (UF) failure. However, the impact of intraperitoneal pressure (IPP) on the peritoneum remains unclear.


In this study, we employed a mouse PD model and human Met-5A cells to investigate the influence of pressure on the peritoneum and mesothelial cells. We utilized repeated, chronic infusion of glucose-free phosphate-buffered saline (PBS) to increase IPP and examined its effects.


We observed that increased IPP induced peritoneal fibrosis and upregulated the expression of cluster of differentiation 44 (CD44) in mesothelial cells (Figure 1). Pressurization led to a mesenchymal phenotype, the expression of fibrotic markers and inflammatory factors, increased cell proliferation, and cell migration in Met-5A cells. The mouse PD model and human peritoneum equilibrium tests showed a positive association between higher IPP and both increased small solute transport and decreased net UF. The treatment of CD44 neutralizing antibodies prevented pressure-induced phenotypic changes in mesothelial cells, while a CD44 inhibitor oligo-fucoidan ameliorated pressure-induced peritoneal thickening, fibrosis, and inflammation in PD mice.


Our findings suggest that IPP plays a crucial role in peritoneal fibrosis in PD. CD44-mediated mesothelial changes and inflammation are involved in these processes. The experiments of CD44 blockade showed its potential as a therapeutic approach for PD-related peritoneal fibrosis and UF failure.

Figure 1. Pressure-induced CD44 expression and peritoneal fibrotic changes, thickening and “stampede” phenomenon.


  • Government Support – Non-U.S.