Relationship of Fibroblast Growth Factor 23 (FGF-23) Serum Levels With Low Bone Mass in Postmenopausal Women

Advanced glycation end products (AGEs) may induce cardiac remodeling in kidney disease by promoting fibroblast growth factor 23 (FGF-23) expression. Since AGEs are increased in diabetes mellitus (DM), our first aim was to evaluate the existence of any potential association between AGEs, FGF-23, inflammation, and increased cardiovascular risk in DM patients on dialysis (CKD-G5D). Secondarily, we explored the potential role of the soluble receptor for AGEs (sRAGE) as a marker of heart failure. Levels of glycated albumin (GA), sRAGE, c-terminal FGF-23 (cFGF-23), brain natriuretic peptide (BNP), and inflammatory mediators were compared between DM and non-DM CKD-G5D patients. The levels of sRAGE, cFGF-23, BNP, and proinflammatory markers were over the ranges of normality in both DM and non-DM groups. Only GA and sRAGE levels were increased in DM compared to non-DM patients. Plasma levels of sRAGE and CRP were the only independent predictors of BNP concentration. In conclusion, in DM CKD-G5D patients, sRAGE appeared to be a marker of cardiac remodeling. Indeed, its increase could be a potential protective mechanism against the increased risk of cardiovascular complications related to AGEs and inflammation. The causal relationship between sRAGE and cardiovascular risk in these patients needs to be further confirmed by mechanistic studies.

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Fibroblast growth factor-23 (FGF-23) as a prognostic marker for chronic kidney disease (CKD)

Science-Business eXchange ◽

10.1038/scibx.2011.726 ◽

2011 ◽

Vol 4 (25) ◽

pp. 726-726

Keyword(s):

Chronic Kidney Disease ◽

Growth Factor ◽

Kidney Disease ◽

Fibroblast Growth Factor ◽

Prognostic Marker ◽

Fibroblast Growth Factor 23 ◽

Fibroblast Growth ◽

Fgf 23

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MP594THE RELATIONSHIP BETWEEN FIBROBLAST GROWTH FACTOR-23 (FGF-23) AND SELECTED CLINICAL AND LABORATORY PARAMETERS

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfx177.mp594 ◽

2017 ◽

Vol 32 (suppl_3) ◽

pp. iii648-iii649

Author(s):

Danuta Fedak ◽

Marek Kużniewski ◽

Marcin Krzanowski ◽

Paulina Dumnicka ◽

Wladyslaw Sulowicz

Keyword(s):

Growth Factor ◽

Fibroblast Growth Factor ◽

Fibroblast Growth Factor 23 ◽

Fibroblast Growth ◽

Laboratory Parameters ◽

Fgf 23

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Serum fibroblast growth factor-23 (FGF-23) and fracture risk in elderly men

Journal of Bone and Mineral Research ◽

10.1002/jbmr.263 ◽

2011 ◽

Vol 26 (4) ◽

pp. 857-864 ◽

Cited By ~ 68

Author(s):

Majd AI Mirza ◽

Magnus K Karlsson ◽

Dan Mellström ◽

Eric Orwoll ◽

Claes Ohlsson ◽

...

Keyword(s):

Growth Factor ◽

Fracture Risk ◽

Fibroblast Growth Factor ◽

Fibroblast Growth Factor 23 ◽

Fibroblast Growth ◽

Elderly Men ◽

Fgf 23

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Cardiac hypertrophy elevates serum levels of fibroblast growth factor 23

Kidney International ◽

10.1016/j.kint.2018.02.018 ◽

2018 ◽

Vol 94 (1) ◽

pp. 60-71 ◽

Cited By ~ 25

Author(s):

Isao Matsui ◽

Tatsufumi Oka ◽

Yasuo Kusunoki ◽

Daisuke Mori ◽

Nobuhiro Hashimoto ◽

...

Keyword(s):

Growth Factor ◽

Cardiac Hypertrophy ◽

Fibroblast Growth Factor ◽

Fibroblast Growth Factor 23 ◽

Serum Levels ◽

Fibroblast Growth

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SP287SERUM FIBROBLAST GROWTH FACTOR-23 (FGF-23), SOLUBLE KLOTHO (SKLOTHO) AND SCLEROSTIN LEVELS AS MARKERS OF CARDIOVASCULAR COMPLICATIONS IN RUSSIAN PATIENTS WITH END STAGE OF RENAL DISEASE (REGULAR HEMODIALYSIS AND HEMODIAFILTRATION ON LINE)

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfy104.sp287 ◽

2018 ◽

Vol 33 (suppl_1) ◽

pp. i440-i440

Author(s):

Elena Kozhevnikova ◽

Ludmila Milovanova ◽

Victor Fomin ◽

Yuriy Milovanov ◽

Vasiliy Kozlov ◽

...

Keyword(s):

Growth Factor ◽

Renal Disease ◽

Fibroblast Growth Factor ◽

Fibroblast Growth Factor 23 ◽

Cardiovascular Complications ◽

Fibroblast Growth ◽

On Line ◽

End Stage ◽

Fgf 23 ◽

Regular Hemodialysis

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Fibroblast Growth Factor 23-Producing Phosphaturic Mesenchymal Tumor with Extraordinary Morphology Causing Oncogenic Osteomalacia

Medicina ◽

10.3390/medicina56010034 ◽

2020 ◽

Vol 56 (1) ◽

pp. 34

Author(s):

Cornelia Then ◽

Evelyn Asbach ◽

Harald Bartsch ◽

Niklas Thon ◽

Christian Betz ◽

...

Keyword(s):

Growth Factor ◽

Fibroblast Growth Factor ◽

Fibroblast Growth Factor 23 ◽

Olfactory Neuroblastoma ◽

Mesenchymal Tumor ◽

Fibroblast Growth ◽

Phosphaturic Mesenchymal Tumor ◽

Oncogenic Osteomalacia ◽

Pet Ct ◽

Fgf 23

A possible cause of hypophosphatemia is paraneoplastic secretion of fibroblast growth factor 23 (FGF-23). Tumors secreting FGF-23 are rare, mostly of mesenchymal origin, usually benign, and may be located anywhere in the body, including hands and feet, which are often not represented in conventional imaging. A 50-year-old woman presented with diffuse musculoskeletal pain and several fractures. Secondary causes of osteoporosis were excluded. Laboratory analysis revealed hypophosphatemia and elevated alkaline phosphatase, parathyroid hormone, and FGF-23. Thus, oncogenic osteomalacia due to neoplastic FGF-23 secretion was suspected. FDG-PET-CT and DOTATATE-PET-CT imaging demonstrated no tumor. Cranial MRI revealed a tumorous mass in the left cellulae ethmoidales. The tumor was resected and histopathological examination showed a cell-rich tumor with round to ovoid nuclei, sparse cytoplasm, and sparse matrix, resembling an olfactory neuroblastoma. Immunohistochemical analysis first led to diagnosis of olfactory neuroblastoma, which was later revised to phosphaturic mesenchymal tumor. Following the resection, FGF-23 and phosphate levels normalized. In conclusion, we here describe a patient with an FGF-23-secreting phosphaturic mesenchymal tumor with an unusual morphology. Furthermore, we emphasize diagnostic pitfalls when dealing with FGF-23-induced hypophosphatemia.

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Fibroblast growth factor-23 is associated with imaging markers of diabetic cardiomyopathy and anti-diabetic therapeutics

Cardiovascular Diabetology ◽

10.1186/s12933-020-01135-z ◽

2020 ◽

Vol 19 (1) ◽

Author(s):

Martin H. Sørensen ◽

Annemie S. Bojer ◽

Niklas R. Jørgensen ◽

David A. Broadbent ◽

Sven Plein ◽

...

Keyword(s):

Type 2 Diabetes ◽

Growth Factor ◽

Fibroblast Growth Factor ◽

Kidney Function ◽

Fibroblast Growth Factor 23 ◽

Left Ventricular ◽

Fibroblast Growth ◽

Cardiovascular Morbidity And Mortality ◽

Fgf 23

Abstract Background The biomarker fibroblast growth factor-23 (FGF-23) has been associated with increased cardiovascular morbidity and mortality in both patients with and without type 2 diabetes. The aim of this study was to evaluate the relationship between FGF-23 and cardiac structure, function and perfusion in patients with type 2 diabetes and normal or mildly impaired kidney function. Furthermore, to investigate the association between FGF-23, anti-diabetes therapy and the classic complications and risk factors associated with type 2 diabetes. Methods In this cross-sectional study, 246 patients with type 2 diabetes underwent echocardiography and advanced cardiac magnetic resonance imaging to assess left ventricular (LV) structure and function. In addition, myocardial blood flow (MBF) during rest and pharmacological stress (adenosine 140 µg/kg/min) were evaluated in 183 of the patients. Patients with eGFR < 60 ml/min/1.73 m2 were excluded. Results Median (Q1–Q3) FGF-23 was 74 (58–91) ng/L. Patients with FGF-23 above the median had lower MBF during stress (2.3 ± 0.9 vs. 2.7 ± 0.9 ml/min/g, P = 0.001) and lower overall myocardial perfusion reserve (MPR) (2.7 ± 0.8 vs. 3.3 ± 1.1, P < 0.001). LV mass (143 ± 40 vs. 138 ± 36 g, P = 0.04) and E/e* (8.5 ± 3.2 vs. 7.6 ± 2.7, P = 0.04) were higher in patients with FGF-23 above the median. In a linear model adjusted for age, sex, eGFR and hypertension, increasing FGF-23 was associated with decreased MPR (P < 0.01, R2 = 0.11) and increased E/e* (P < 0.01, R2 = 0.07). FGF-23 was lower in patients receiving glucagon like peptide-1 (GLP-1) analogues (71 (57–86) vs. 80 (60–98) ng/L, P = 0.01) than in those who did not receive GLP-1 analogues. Conclusions In patients with type 2 diabetes and normal or mildly impaired kidney function, increased levels of FGF-23 are associated with impaired cardiac diastolic function and decreased MPR, caused by a decrease in maximal MBF during stress. Use of GLP-1 analogues is associated with decreased levels of FGF-23. Clinical trial registrationhttps://www.clinicaltrials.gov. Unique identifier: NCT02684331. Date of registration: February 18, 2016

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Regulation of serum 1,25(OH)2Vitamin D3 levels by fibroblast growth factor 23 is mediated by FGF receptors 3 and 4

AJP Renal Physiology ◽

10.1152/ajprenal.00740.2010 ◽

2011 ◽

Vol 301 (2) ◽

pp. F371-F377 ◽

Cited By ~ 62

Author(s):

Jyothsna Gattineni ◽

Katherine Twombley ◽

Regina Goetz ◽

Moosa Mohammadi ◽

Michel Baum

Keyword(s):

Vitamin D ◽

Growth Factor ◽

Fibroblast Growth Factor ◽

Fibroblast Growth Factor 23 ◽

Serum Levels ◽

Phosphate Transport ◽

Fibroblast Growth ◽

Wild Type ◽

Baseline Serum ◽

Renal Phosphate Reabsorption

Fibroblast growth factor 23 (FGF23) is a phosphaturic hormone implicated in the pathogenesis of several hypophosphatemic disorders. FGF23 causes hypophosphatemia by decreasing the expression of sodium phosphate cotransporters (NaPi-2a and NaPi-2c) and decreasing serum 1,25(OH)2Vitamin D3 levels. We previously showed that FGFR1 is the predominant receptor for the hypophosphatemic actions of FGF23 by decreasing renal NaPi-2a and 2c expression while the receptors regulating 1,25(OH)2Vitamin D3 levels remained elusive. To determine the FGFRs regulating 1,25(OH)2Vitamin D3 levels, we studied FGFR3−/−FGFR4−/− mice as these mice have shortened life span and are growth retarded similar to FGF23−/− and Klotho−/− mice. Baseline serum 1,25(OH)2Vitamin D3 levels were elevated in the FGFR3−/−FGFR4−/− mice compared with wild-type mice (102.2 ± 14.8 vs. 266.0 ± 34.0 pmol/l; P = 0.001) as were the serum levels of FGF23. Administration of recombinant FGF23 had no effect on serum 1,25(OH)2Vitamin D3 in the FGFR3−/−FGFR4−/− mice (173.4 ± 32.7 vs. 219.7 ± 56.5 pmol/l; vehicle vs. FGF23) while it reduced serum 1,25(OH)2Vitamin D3 levels in wild-type mice. Administration of FGF23 to FGFR3−/−FGFR4−/− mice resulted in a decrease in serum parathyroid hormone (PTH) levels and an increase in serum phosphorus levels mediated by increased renal phosphate reabsorption. These data indicate that FGFR3 and 4 are the receptors that regulate serum 1,25(OH)2Vitamin D3 levels in response to FGF23. In addition, when 1,25(OH)2Vitamin D3 levels are not affected by FGF23, as in FGFR3−/−FGFR4−/− mice, a reduction in PTH can override the effects of FGF23 on renal phosphate transport.

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