Possible involvement of circulating fibroblast growth factor 23 in the development of secondary hyperparathyroidism associated with renal insufficiency

Recovery of Hyperphosphatoninism and Renal Phosphorus Wasting One Year after Successful Renal Transplantation

“…Apparently, inappropriate hyperphosphatoninism fades away by 1 yr after successful transplantation. As in CKD patients (9,13,24), renal function was a major determinant of FGF-23 serum levels in RTR at M12. Parameters included in the model: FGF-23 pre , serum albumin-corrected calcium, phosphorus, PTH, calcidiol, calcitriol alkaline phosphatases, and eGFR.…”

“…These findings indicate that in progressive renal failure compensatory increases in renal phosphorus excretion are recruited before the development of hyperphosphatemia. This increase in renal phosphorus excretion is driven, at least partly, by parathyroid hormone (PTH) and by FGF-23 (9,(11)(12)(13). Renal transplant recipients (RTR) represent a unique subset of patients with CKD.…”

Fibroblast Growth Factor-23 in Early Chronic Kidney Disease

“…Recent clinical studies demonstrate a high fractional renal phosphate excretion despite the presence of normophosphatemia in early CKD (2)(3)(4). The increased renal phosphate excretion is driven, at least partly, by parathyroid hormone (PTH) and fibroblast growth factor-23 (FGF-23) (3,(5)(6)(7).…”

FGF-23: estado da arte

“…39 Several studies have shown the correlation between the serum levels of FGF-23 and creatinine, P and PTH in patients with nondialysis CKD. [40][41][42][43] The levels of that hormone increases as renal function decreases. 41 Even in patients with a glomerular filtration rate higher than 80 mL/min, FGF-23 levels correlate negatively with 1α,25(OH) 2 D 3 and P tubular reabsorption.…”