The effects of iron on FGF23-mediated Ca–P metabolism in CKD patients

Deger, Serpil Muge; Erten, Yasemin; Paşaoğlu, Özge Tuğçe; Derici, Ülver; Reis, Kadriye Altok; Öneç, Kürşad; Paşaoğlu, Hatîce

doi:10.1007/s10157-012-0725-0

Cited by 24 publications

(17 citation statements)

References 21 publications

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“…But in this study there was no data about the association of hemoglobin and iFGF-23 46 . Researchers think some carbohydrate components in iron preparations to inhibit FGF-23 degradation in osteocytes to cause a transient raise in iFGF-23 [44][45][46] . In another study iron isomaltose and FCM given intraperitoneally were shown to have no effect on plasma iFGF23 levels both in normal and uremic rats 47 .…”

Section: Discussioncontrasting

confidence: 56%

Fibroblast growth factor is associated to left ventricular mass index, anemia and low values of transferrin saturation

et al. 2015

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Section: Discussioncontrasting

confidence: 56%

Fibroblast growth factor is associated to left ventricular mass index, anemia and low values of transferrin saturation

et al. 2015

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“…60 This is likely due to the role of iron and iron-related pathways in FGF23 synthesis and processing mechanisms. 61 As a consequence of this regulatory action and the negative association between iron therapy and FGF23 serum levels documented in dialysis patients, 62 iron administration per se and also treatment with iron-based phosphate binders may be helpful in the control of bone metabolism decreasing FGF23 both directly and by reducing phosphate intestinal absorption.…”

Section: Resultsmentioning

confidence: 99%

Phosphate binders for the treatment of chronic kidney disease: role of iron oxyhydroxide

Cernaro

Santoro

Lacquaniti

et al. 2016

IJNRD

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Chronic kidney disease-mineral bone disorder is frequent in patients with renal failure. It is characterized by abnormalities in mineral and bone metabolism with resulting hyperphosphatemia, low serum vitamin D, secondary hyperparathyroidism, altered bone morphology and strength, higher risk of bone fractures, and development of vascular or other soft tissue calcifications. Besides the recommendation to reduce phosphorus dietary intake, many drugs are currently available for the treatment of calcium/phosphate imbalance. Among them, phosphate binders represent a milestone. Calcium-based binders (calcium carbonate, calcium acetate) are effective in lowering serum phosphate, but their use has been associated with an increased risk of hypercalcemia and calcifications. Calcium-free binders (sevelamer hydrochloride, sevelamer carbonate, and lanthanum carbonate) are equally or slightly less effective than calcium-containing compounds. They would not induce an increase in calcium levels but may have relevant side effects, including gastrointestinal symptoms for sevelamer and risk of tissue accumulation for lanthanum. Accordingly, new phosphate binders are under investigation and some of them have already been approved. A promising option is sucroferric oxyhydroxide (Velphoro ® , PA21), an iron-based phosphate binder consisting of a mixture of polynuclear iron(III)-oxyhydroxide, sucrose, and starches. The present review is focused on pharmacology, mode of action, and pharmacokinetics of sucroferric oxyhydroxide, with a discussion on comparative efficacy, safety, and tolerability studies of this drug in chronic kidney disease and patient perspectives such as quality of life, satisfaction, and acceptability. Sucroferric oxyhydroxide has proven to be as effective as sevelamer in reducing phosphatemia with a similar safety profile and lower pill burden. Experimental and clinical studies have documented a minimal percentage of iron absorption without inducing toxicity. In conclusion, the overall benefit-risk balance of sucroferric oxyhydroxide is deemed to be positive, and this new drug may therefore represent a good alternative to traditional phosphate binders for the treatment of hyperphosphatemia in dialysis patients.

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“…Takeda et al observed that intravenous administration of saccharated ferric oxide caused only a small increase of already elevated iFGF23 concentrations [10]. In contrast, Deger et al showed a negative correlation between iron supplementation and iFGF23 level in dialysis patients [11]. In non-CKD children with endemic iron deficiency, an improvement in iron status following supplementation was associated with a significant decrease in circulating cFGF23 concentration [12].…”

Section: Introductionmentioning

confidence: 95%

Plasma fibroblast growth factor 23 concentration and iron status. Does the relationship exist in the elderly population?

Bożentowicz-Wikarek¹,

Kocełak²,

Owczarek³

et al. 2015

Clinical Biochemistry

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The effects of iron on FGF23-mediated Ca–P metabolism in CKD patients

Cited by 24 publications

References 21 publications

Fibroblast growth factor is associated to left ventricular mass index, anemia and low values of transferrin saturation

Fibroblast growth factor is associated to left ventricular mass index, anemia and low values of transferrin saturation

Phosphate binders for the treatment of chronic kidney disease: role of iron oxyhydroxide

Plasma fibroblast growth factor 23 concentration and iron status. Does the relationship exist in the elderly population?

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