Regulation of serum phosphate

Lederer, Eleanor

doi:10.1113/jphysiol.2014.273979

Cited by 123 publications

(92 citation statements)

References 71 publications

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“…These results may also contradict the findings of several other studies where a significant effect of an increased production and secretion of FGF23 on serum PTH was seen and was either phosphate mediated or independent [37, 38]. It seems that our study might have been too short to demonstrate any changes of PTH.…”

Section: Discussioncontrasting

confidence: 56%

Associations Between Intravenous Iron, Inflammation and FGF23 in Non-Dialysis Patients with Chronic Kidney Disease Stages 3-5

Muras-Szwedziak¹,

Nowicki²

2018

Kidney Blood Press Res

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Background/Aims: Both iron deficiency and chronic inflammation are highly prevalent in patients with chronic kidney disease (CKD). The effect of intravenous iron infusion on mineral metabolism in CKD may be modified by inflammation. Intravenous iron theraphy may reduce peripheral degradation, secretion, clearence of iFGF23 and lead to hypophosphatemia. The aim of the study was to evaluate the effect of intravenous iron on mineral metabolism in CKD patients. Methods: 35 non-dialysis patients with CKD stages 3-5. received 100 mg/24h of ferric oxide saccharated solution for 5 days. Serum calcium (Ca), phosphorus (P), parathormone (PTH), intact-FGF23 (iFGF23), C-terminal-FGF23 (cFGF23), bone alkaline phosphatase (BAP) and high-sensitive CRP were assessed on day 1 and 3 at baseline and 2 hours after each dose administration and once on day 6. Plasma iFGF23 and cFGF23, as well as serum BAP were measured with ELISA and other parameters with standard automated laboratory methods. Results: Serum iFGF23 increased after iv iron on day 1 and 6 (from 268.9±446.5 to 326.3±529.9 on day 1; p=0.05 and to 451.4±601 pg/mL on day 6; p=0.03). cFGF23 was reduced only on day 1 (from 654.3±441.3 to 473.6±414 RU/mL; p=0.016). P concentration decreased significantly two hours after the first iron infusion (from 1.69±0.5 to 1.54±0.35 mmol/l; p=0.003). In following days the changes of cFGF23, P and of other calcium-phosphate metabolism were not significant. Serum CRP correlated neither with iFGF-23 nor cFGF-23. Conclusion: Intravenous iron supplementation may only transiently affect the production and degradation of FGF23 resulting in hypophosphatemia at the commencement of iron therapy. Chronic low-grade inflammation does not seem to play a role in that mechanism.

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Section: Discussioncontrasting

confidence: 56%

Associations Between Intravenous Iron, Inflammation and FGF23 in Non-Dialysis Patients with Chronic Kidney Disease Stages 3-5

Muras-Szwedziak¹,

Nowicki²

2018

Kidney Blood Press Res

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“…2A) (21). Early fractions from serial BAL of the Npt2b-deficient mouse revealed an opalescent and foamy appearance, consistent with the presence of surfactant material, and examination of total protein and surfactant protein D (SP-D) revealed elevated levels in the BALF (Fig.…”

Section: Resultsmentioning

confidence: 99%

Modeling pulmonary alveolar microlithiasis by epithelial deletion of the Npt2b sodium phosphate cotransporter reveals putative biomarkers and strategies for treatment

et al. 2015

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Pulmonary alveolar microlithiasis (PAM) is a rare, autosomal recessive lung disorder associated with progressive accumulation of calcium phosphate microliths. Inactivating mutations in SLC34A2, which encodes the NPT2b sodium-dependent phosphate cotransporter, has been proposed as a cause of PAM. We show that epithelial deletion of Npt2b in mice results in a progressive pulmonary process characterized by diffuse alveolar microlith accumulation, radio-graphic opacification, restrictive physiology, inflammation, fibrosis, and an unexpected alveolar phospholipidosis. Cytokine and surfactant protein elevations in the alveolar lavage and serum of PAM mice and confirmed in serum from PAM patients identify serum MCP-1 (monocyte chemotactic protein 1) and SP-D (surfactant protein D) as potential biomarkers. Microliths introduced by adoptive transfer into the lungs of wild-type mice produce marked macrophagerich inflammation and elevation of serum MCP-1 that peaks at 1 week and resolves at 1 month, concomitant with clearance of stones. Microliths isolated by bronchoalveolar lavage readily dissolve in EDTA, and therapeutic whole-lung EDTA lavage reduces the burden of stones in the lungs. A low-phosphate diet prevents microlith formation in young animals and reduces lung injury on the basis of reduction in serum SP-D. The burden of pulmonary calcium deposits in established PAM is also diminished within 4 weeks by a low-phosphate diet challenge. These data support a causative role for Npt2b in the pathogenesis of PAM and the use of the PAM mouse model as a preclinical platform for the development of biomarkers and therapeutic strategies.

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“…PTH also modulates bone turnover, contributing to calcium and phosphate homeostasis of the skeleton 32 . In early stage of hyperparathyroidism, PTH stimulates bone release of calcium and phosphate, enhances intestinal absorption of calcium and phosphate, and increases renal calcium reabsorption while decreasing urinary phosphate reabsorption, thus maintaining a relatively normal serum phosphate concentration 33 . High PTH can stimulate the secretion of 1,25-(OH) 2 vitamin D and FGF23 12 .…”

Section: Overview Of Phosphate Homeostasismentioning

confidence: 99%

Alpha Klotho and phosphate homeostasis

Bian

Xing

2014

J Endocrinol Invest

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The Klotho family consists of three single-pass transmembrane proteins—αKlotho, βKlotho and γKlotho. Each of them combines with fibroblast growth factor (FGF) receptors (FGFRs) to form receptor complexes for various FGF’s. αKlotho is a co-receptor for physiological FGF23 signaling and appears essential for FGF23-mediated regulation of mineral metabolism. αKlotho protein also plays a FGF23-independent role in phosphate homeostasis. Animal experimental studies and clinical observations have demonstrated that αKlotho deficiency leads to severe hyperphosphatemia; moderate elevation of αKlotho reduces serum phosphate and extremely high αKlotho induces hypophosphatemia and high-FGF23. αKlotho maintains circulating phosphate in a narrow range by modulating intestinal phosphate absorption, urinary phosphate excretion by the kidney, and phosphate distribution into bone rather than soft tissue in concerted interaction with other calciophosphotropic hormones such as PTH, FGF23, and 1,25-(OH)2 vitamin D. The role of αKlotho in maintenance of phosphate homeostasis is mediated by direct suppression of Na-dependent phosphate cotransporters in target organs. Therefore, αKlotho manipulation may be a novel strategy for genetic and acquired phosphate disorders and for medical conditions with αKlotho deficiency such as chronic kidney disease in future.

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Regulation of serum phosphate

Cited by 123 publications

References 71 publications

Associations Between Intravenous Iron, Inflammation and FGF23 in Non-Dialysis Patients with Chronic Kidney Disease Stages 3-5

Associations Between Intravenous Iron, Inflammation and FGF23 in Non-Dialysis Patients with Chronic Kidney Disease Stages 3-5

Modeling pulmonary alveolar microlithiasis by epithelial deletion of the Npt2b sodium phosphate cotransporter reveals putative biomarkers and strategies for treatment

Alpha Klotho and phosphate homeostasis

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