Study of Fibroblast Growth Factor 23(FGF23) in the Early Post Renal Transplantation Period

Abstract

FGF23 is free circulating endocrine hormone which Secreted by osteocytes. FGF23 affect phosphate metabolism mainly as it inhibits renal tubular phosphat reabsorption by suppressing the expression of luminal sodium– phosphate co-transporters (NaPi). Increased FGF23 is independently associated with arterial stiffness, endothelial dysfunction and increased ventricular mass through direct activation of GF23 receptor present in cardiac tissue and this action is Koltho independent because Koltho co receptor not expressed in myocardial cell After renal transplantation the residual FGF23 activity may also contribute to early post-transplant hypophosphatemia, which could in turn play a role in the pathogenesis of post-transplant bone disease. Post-transplantation hypophosphataemia can have a detrimental effect on bone mineralization and might contribute to impaired osteoblast genesis and early osteoblast apoptosis, which further contributes to post-transplantation osteoporosis. Data from bone biopsies obtained from renal transplant recipients after transplantation have shown that serum phosphate levels are lower in patients with early osteoblast apoptosis, with serum phosphate levels correlating positively with osteoblast number and correlating negatively with the number of apoptotic osteoblasts. Also high FGF-23 levels were associated with a reduction in BMD in the lumbar spine and total hip regions during the first year post-transplantation.