Fibroblast growth factor 23: are we ready to use it in clinical practice?

Krijger, Annet Bouma-de; Vervloet, Marc G.

doi:10.1007/s40620-020-00715-2

Cited by 26 publications

(25 citation statements)

References 151 publications

(220 reference statements)

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“…As kidney function decreases, the level of FGF-23 concentration in serum gradually increases and reaches its maximum value in the end-stage kidney disease [ 12 , 13 ]. Moreover, positive correlations of FGF-23 with high mortality risk due to cardiovascular complications, as well as with independent left ventricular hypertrophy were reported in CKD adult populations [ 14 , 15 , 16 ]. Likewise, different correlations between FGF-23 and kidney function, calcium, phosphate, parathyroid hormone (PTH), and vitamin D have been shown in pediatric studies, which are limited in the literature [ 17 , 18 , 19 , 20 ].…”

Section: Introductionmentioning

confidence: 99%

FGF-23 and Phosphate in Children with Chronic Kidney Disease: A Cross-Sectional Study in Kazakhstan

et al. 2020

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Background and objectives: Chronic kidney disease (CKD) in children is a complex medical and social issue around the world. One of the serious complications is mineral-bone disorder (CKD-MBD) which might determine the prognosis of patients and their quality of life. Fibroblast growth factor 23 (FGF-23) is a phosphaturic hormone which is involved in the pathogenesis of CKD-MBD. The purpose of the study was to determine what comes first in children with CKD: FGF-23 or phosphate. Materials and Methods: This cross-sectional study included 73 children aged 2–18 years with CKD stages 1–5. We measured FGF-23 and other bone markers in blood samples and studied their associations. Results: Early elevations of FGF-23 were identified in children with CKD stage 2 compared with stage 1 (1.6 (1.5–1.8) pmol/L versus 0.65 (0.22–1.08), p = 0.029). There were significant differences between the advanced stages of the disease. FGF-23 correlated with PTH (r = 0.807, p = 0.000) and phosphate (r = 0.473, p = 0.000). Our study revealed that the elevated level of FGF-23 went ahead hyperphosphatemia and elevated PTH. Thus, more than 50% of children with CKD stage 2 had the elevating level of serum FGF-23, and that index became increasing with the disease progression and it achieved 100% at the dialysis stage. The serum phosphate increased more slowly and only 70.6% of children with CKD stage 5 had the increased values. The PTH increase was more dynamic. Conclusions: FGF-23 is an essential biomarker, elevates long before other markers of bone metabolism (phosphate), and might represent a clinical course of disease.

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Section: Introductionmentioning

confidence: 99%

FGF-23 and Phosphate in Children with Chronic Kidney Disease: A Cross-Sectional Study in Kazakhstan

et al. 2020

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“…FGF23 is more and more identified to be a cardiovascular-related detrimental factor ( 21–23 ), and several strategies to reduce FGF23 levels have been studied extensively ( 24 ). Interestingly, recent studies suggest that lower potassium intake is associated with a higher FGF23 level ( 25 ) and that changes in potassium or sodium homeostasis may influence bone and mineral parameters and bone health ( 26–29 ).…”

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confidence: 99%

Effects of Potassium or Sodium Supplementation on Mineral Homeostasis: A Controlled Dietary Intervention Study

Humalda

Yeung

Geleijnse

et al. 2020

The Journal of Clinical Endocrinology &Amp; Metabolism

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Context Although dietary potassium and sodium intake may influence calcium-phosphate metabolism and bone health, the effects on bone mineral parameters, including fibroblast growth factor 23 (FGF23), are unclear. Objective Here, we investigated the effects of potassium or sodium supplementation on bone mineral parameters. Design, setting, participants We performed a post hoc analysis of a dietary controlled randomized, blinded, placebo-controlled crossover trial. Prehypertensive individuals not using antihypertensive medication (n = 36) received capsules containing potassium chloride (3 g/d), sodium chloride (3 g/d), or placebo. Linear mixed-effect models were used to estimate treatment effects. Results Potassium supplementation increased plasma phosphate (from 1.10 ± 0.19 to 1.15 ± 0.19 mmol/L, P = 0.004), in line with an increase in tubular maximum of phosphate reabsorption (from 0.93 ± 0.21 to 1.01 ± 0.20 mmol/L, P < 0.001). FGF23 decreased (114.3 [96.8-135.0] to 108.5 [93.5-125.9] RU/mL, P = 0.01), without change in parathyroid hormone and 25-hydroxy vitamin D3. Fractional calcium excretion decreased (from 1.25 ± 0.50 to 1.11 ± 0.46 %, P = 0.03) without change in plasma calcium. Sodium supplementation decreased both plasma phosphate (from 1.10 ± 0.19 to 1.06 ± 0.21 mmol/L, P = 0.03) and FGF23 (from 114.3 [96.8-135.0] to 108.7 [92.3-128.1] RU/mL, P = 0.02). Urinary and fractional calcium excretion increased (from 4.28 ± 1.91 to 5.45 ± 2.51 mmol/24 hours, P < 0.001, and from 1.25 ± 0.50 to 1.44 ± 0.54 %, P = 0.004, respectively). Conclusions Potassium supplementation led to a decrease in FGF23, which was accompanied by increase in plasma phosphate and decreased calcium excretion. Sodium supplementation reduced FGF23, but this was accompanied by decrease in phosphate and increase in fractional calcium excretion. Our results indicate distinct effects of potassium and sodium intake on bone mineral parameters, including FGF23. Clinical Trial Registration number NCT01575041

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“…The FGF-receptor- α -Klotho complex in the distal renal tubule is the primary target for FGF23. In the kidney, FGF23 inhibits the production of the sodium phosphate cotransporters Npt2a and Npt2c, which increases phosphate reabsorption in the proximal renal tubule (phosphating effect) [ 10 ]. In addition, FGF23 suppresses the expression of 1- α -hydrolase, resulting in a decrease in active vitamin D formation.…”

Section: Mechanisms Of Action Of Fgf23mentioning

confidence: 99%

FGF23: A Review of Its Role in Mineral Metabolism and Renal and Cardiovascular Disease

et al. 2021

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FGF23 is a hormone secreted mainly by osteocytes and osteoblasts in bone. Its pivotal role concerns the maintenance of mineral ion homeostasis. It has been confirmed that phosphate and vitamin D metabolisms are related to the effect of FGF23 and its excess or deficiency leads to various hereditary diseases. Multiple studies have shown that FGF23 level increases in the very early stages of chronic kidney disease (CKD), and its concentration may also be highly associated with cardiac complications. The present review is limited to some of the most important aspects of calcium and phosphate metabolism. It discusses the role of FGF23, which is considered an early and sensitive marker for CKD-related bone disease but also as a novel and potent cardiovascular risk factor. Furthermore, this review gives particular attention to the reliability of FGF23 measurement and various confounding factors that may impact on the clinical utility of FGF23. Finally, this review elaborates on the clinical usefulness of FGF23 and evaluates whether FGF23 may be considered a therapeutic target.

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Fibroblast growth factor 23: are we ready to use it in clinical practice?

Cited by 26 publications

References 151 publications

FGF-23 and Phosphate in Children with Chronic Kidney Disease: A Cross-Sectional Study in Kazakhstan

FGF-23 and Phosphate in Children with Chronic Kidney Disease: A Cross-Sectional Study in Kazakhstan

Effects of Potassium or Sodium Supplementation on Mineral Homeostasis: A Controlled Dietary Intervention Study

FGF23: A Review of Its Role in Mineral Metabolism and Renal and Cardiovascular Disease

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