Abstract: TH-PO519
Effect of Acute Peritonitis on Serum Fibroblast Growth Factor 23 in a Rat Model of CKD: Possible Interaction Between FGF-23 and Inflammation
Session Information
- Bone and Mineral Metabolism: Basic
November 07, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Bone and Mineral Metabolism
- 401 Bone and Mineral Metabolism: Basic
Authors
- Ramadan, Nagwa Mahmoud, Faculty of Medicine, Cairo University, Giza, Cairo, Egypt
- Mubarak, Hanan A., Faculty of Medicine, Cairo University, Giza, Cairo, Egypt
- Yacoub, Christina Sabry, Faculty of Medicine, Cairo University, Giza, Cairo, Egypt
- Elsebaie, Mohamed Mahmoud, Faculty of medicine cairo University Egypt, Cairo, Egypt
- Osman, Noha, Kasr AlAiny School of Medicine, Cairo University, Giza, Cairo, Egypt
- Nasrallah, Mohamed M., Kasr AlAiny School of Medicine, Cairo University, Giza, Cairo, Egypt
Background
Cardiovascular diseases are the leading cause of death among patients with chronic kidney disease (CKD). Fibroblast Growth Factor 23 (FGF- 23) has been associated with mortality among those patients and was found to correlate with different parameters of inflammation among them. The interaction between FGF- 23, uremia and inflammation is still under investigation.
Methods
40 rats assigned to 4 groups: Control sham-operated, Acute peritonitis, CKD and CKD + acute peritonitis. Acute peritonitis and CKD were experimentally induced. Serum creatinine, phosphorus, iFGF23,Vit.D, TNFa, HsCRP and bone furin mRNA were compared between groups.
Results
Compared to the control group; FGF- 23 was significantly higher in both the CKD & the acute peritonitis groups. FGF 23 reached the highest level in the CKD with induced acute peritonitis group . Furin mRNA was significantly lower in both the CKD and the acute peritonitis groups compared to the control group and it reached its lowest levels in the group with induced CKD and peritonitis. FGF- 23 was positively correlated to serum creatinine, phosphorus, TNFa&CRP while it was negatively correlated to serum Vit.D & Furin mRNA.
Conclusion
Inflammation is a potent upregulator of iFGF23 and could be a main promoter of FGF23 excess early in CKD. Acute peritonitis on top of CKD amplifies the inflammatory states which could contribute to worsening the clinical outcomes. Increased serum iFGF23 in inflammation could be due to decrease its cleavage by furin pro-protein convertase enzyme.