Thesis (M.Sc.) - Cairo University - Faculty of Medicine - Department of Physiology

Fibroblast growth factor 23(FGF23), a bone-derived hormone that regulates phosphate and vitamin D homeostasis, found to be increased during chronic inflammation of chronic kidney disease (CKD). It is thought to be a causal factor of cardiovascular complications, CKD progression and death. So, understanding the molecular mechanisms that control FGF23 is a critical to design therapy for lowering FGF23 in CKD. The aim of the present study was to explore the effect of acute inflammation on serum FGF23 in CKD, to investigate whether the expression of furin pro-protein convertase enzyme is altered by inflammation in CKD and to clarify the difference in the biological response (regarding FGF23 levels & processing) to acute inflammation versus chronic adaptation to inflammatory stimuli in CKD and to explore the interaction between FGF23, Vitamin D and inflammation. Forty male albino rats were divided into four groups, ten rats for each group, group I: control rats, group II: experimentally induced acute peritonitis, group III: experimentally induced chronic kidney disease (CKD), group IV: CKD with acute peritonitis. The serum levels of creatinine, phosphates, intact (iFGF23), vitamin D, Tumor necrosis factor alpha (TNFa) and C-reactive protein (CRP) were measured. Also, Furin mRNA was measured in femur bone tissue. Results revealed that peritonitis significantly increased serum iFGF23, TNFa and CRP levels; meanwhile, it induced significant decrease in serum vitamin D level and bone furin mRNA compared to the control group. CKD whether alone or with peritonitis significantly increased serum creatinine, phosphate, iFGF23, TNFa and CRP levels; meanwhile, they induced significant decrease in serum vitamin D level and furin mRNA compared to the control group

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