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Abstract: SA-PO717

Lithium-Mediated Protection of Mesothelial Cells during Peritoneal Dialysis

Session Information

  • Peritoneal Dialysis - II
    November 04, 2017 | Location: Hall H, Morial Convention Center
    Abstract Time: 10:00 AM - 10:00 AM

Category: Dialysis

  • 608 Peritoneal Dialysis


  • Herzog, Rebecca, Medical University of Vienna, Vienna, Austria
  • Bialas, Katarzyna, Medical University of Vienna, Vienna, Austria
  • Aufricht, Christoph, Medical University of Vienna, Vienna, Austria
  • Kratochwill, Klaus, Medical University of Vienna, Vienna, Austria

Peritoneal mesothelial cells (MC) are harmed by peritoneal dialysis fluids (PDF), at least in part caused by inadequate cellular stress responses. In immortalized MC, we have shown that addition of lithium chloride (LiCl) restored heat shock protein expression. Lithium salts could therefore be a promising group of molecules to be used as cytoprotective additives to PDF. Here, we analyzed the protective potential of LiCl in human primary MC (HPMC) on the gene and protein expression level in a multi-omics approach and in-vivo in a chronic mouse model of PD.


HPMC of 5 individual donors were exposed to PDF (Extraneal, Baxter) without or with 2.5 or 10mM LiCl 30 min and allowed to recover for 4 or 16 h. Cell death was analyzed by LDH-release. mRNA levels were analyzed by gene expression microarrays and significantly altered biological processes were identified using the PANTHER database. Changes of the proteome were analyzed with a 2D difference gel electrophoresis (DiGE) based approach. C57/B6 mice (n=32) were treated with PDF without or with 5mM LiCl for four weeks via an implanted catheter. The parietal peritoneum was analyzed for thickening/fibrosis and effluent cells were characterized following a 30 min dwell by FACS.


PDF-induced cell injury was associated with significantly differential expression of 601 genes compared to control. Six biological pathways (oxidative stress response, VEGF signaling, PDGF signaling, angiogenesis, CCKR signaling, GNRHR pathway) were significantly overrepresented. Added LiCl led to significantly decreased cell death and significantly altered the expression of 1003 genes, of which 62 showed an abolishment of the PDF-effects. These genes are regarded as markers of LiCl-mediated cytoprotection. In-vivo LiCl lead to a decrease of PDF-induced peritoneal membrane thickening and increased Treg/IL-17 ratio of the effluent cells.


The cytoprotective effects of added LiCl, combined with the modulation of the cellular stress response, fibrosis and inflammation suggests a therapeutic potential of this intervention. Future studies including pharmacokinetics following once daily exposure to LiCl added to Extraneal are needed to further translate these findings into the clinical setting of PD.


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