Serum fibroblast growth factor-23 levels predict the future refractory hyperparathyroidism in dialysis patients

Abstract

Serum FGF-23 level was found to be the most useful factor in predicting future development of refractory secondary hyperparathyroidism in long-term dialysis patients with mild secondary hyperparathyroidism. The measurement of serum FGF-23 levels is a promising laboratory examination that can be applied in the clinical practice of uremic secondary hyperparathyroidism.

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

“…This finding and the observation that PTH levels are elevated in hypophosphatemic disorders caused by elevated FGF-23 levels (26) support the hypothesis that FGF-23 is involved in the pathogenesis of hyperparathyroidism. This hypothesis is further corroborated by the observation in dialysis patients that elevated circulating FGF-23 levels directly correlate with PTH levels and predict refractory hyperparathyroidism (27). On the other hand, there is also some evidence that PTH may increase FGF-23 levels (28,29).…”

Le facteur de croissance des fibroblastes 23 et son récepteur Klotho

“…Au cours de la maladie rénale chronique, avant l'entrée en dialyse, la concentration plasmatique de FGF23 semble prédire la rapidité de dégradation de la fonction rénale chez des sujets non diabétiques [34]. Chez les patients dialysés, la concentration plasmatique de FGF23 est très élevée et prédit la survenue d'une hyperparathyroïdie réfractaire [35,36] et elle est associée à une mortalité accrue durant la première année de dialyse indépendamment de la valeur de la phosphatémie [37]. La possibilité d'un effet direct du FGF23 sur l'os est encore controversée.…”

FGF-23: estado da arte

“…By the end of two years, patients who had high FGF-23 levels at the beginning of the study developed more severe forms of secondary hyperparathyroidism, independently of the initial PTH levels. 47 Gutierrez et al have shown that FGF-23 levels were independently associated with the left ventricular mass index and left ventricular hypertrophy in a group of 162 patients with nondialysis CKD. 48 However, further studies seem to be required to clarify if the increase in FGF-23 is only a marker of ventricular hypertrophy or is deleterious to cardiac tissue.…”

“…However, in the long run, excessive FGF-23 could favor negative clinical outcomes, such as the development of secondary hyperparathyroidism, rapid progression to CKD, and a higher mortality rate. [45][46][47][48][49][50] Thus, modulating serum FGF-23 levels can benefit patients, reducing adverse events, especially those related to disorders of the bone and mineral metabolism.…”

“…52 Knowing that Ca overload influences FGF-23 levels can have implications with important clinical outcomes, such as mortality and cardiovascular disease, since several studies have shown the association between high FGF-23 levels and those clinical outcomes. [45][46][47][48][49][50] Considering all those unanswered questions, a recent review on the topic draws attention to the importance of better understanding the role played by P and FGF-23 in CKD, proposing to the nephrological community a randomized, controlled, long-term study using P binders in the early phases of CKD, and analyzing clinical outcomes, such as vascular calcification, bone health, and CKD progression. 69 conclusIons Several studies have consolidated the role of P as a potentially toxic element, associated with increased mortality rate.…”