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      Correlation of Fgf23 and Balp with Bone Mineral Density in Hemodialysis Patients Translated title: korelacija fgf23 i balp sa mineralnom gustinom kostiju kod pacijenata na hemodijalizi

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          Summary

          Background

          Chronic kidney disease (CKD) is associated with numerous complications such as bone mineral disorder. The aim of our study was to analyze the correlation of bone turnover markers with Bone Mineral Density (BMD) measurements in Tunisian end stage renal diseases (ESRD) patients.

          Methods

          This study included 100 ESRD Tunisian patients. Their estimated glomerular filtration rate (eGFR) was < 15 mL × min -1 × (1.73 m 2) -1, which requires hemodialysis. Bone-specific alkaline phosphatase (BALP) serum concentration was determined with a chemiluminescence immunoassay. Fibroblast Growth Factor 23 (FGF23) serum was assessed by Enzyme-Linked Immunosorbent Assay method. The serum levels of 25-Hydroxyvitamin D (25(OH)D), intact parathyroid hormone (iPTH) and Beta cross-laps (CTX) was measured by Electrochemiluminescence Technology. DEXA (dual-energy x-ray absorptiometry) technique was used to evaluate BMD.

          Results

          We observed a statistically significant negative correlation between BALP levels and total body BMD (r = -0.268; P = 0.015) particularly in femoral neck (FN) (r = -0.219; P = 0.037). BALP concentrations were negatively associated with total BMD especially in FN for patients with BMI < 30, FGF23 concentrations were also negatively correlated with BMD in lumbar spine site (LS) (r = -0.209; P = 0.046). For osteopenic patients we found an inverse correlation between 25(OH)D concentrations and BMD in LS position (r = -0.336; P = 0.038). In men group, we have also found a negative correlation between iPTH and total BMD (r = -0.326; P = 0.015). However we found a positive correlation between calcium expression and BMD in LS site (r = 0.270; P = 0.031).

          Conclusions

          FGF23 and BALP can predict bone loss in ESRD through their strong correlation with BMD in LS and FN sites respectively.

          Kratak sadržaj

          Uvod

          Hronično bubrežno oboljenje (CKD) je praćeno brojnim komplikacijama kao što je poremećaj minerala kostiju. Svha ovog izučavanja je bila da analizira korelaciju markera promena u kostima sa mineralnom gustinom kostiju (BMD) i stupnja renalnih oboljenja kod pacijenata u Tunisu.

          Metode

          Proučavanje je uključilo 100 ESRD tuniskih pacijenata. Njihova prosečna brzina glomerularne filtracije (eGFR) bila je < 15 mL × min -1 × (1,73 m 2) -1 što je zahtevalo hemodijalizu. Koštana alkalna fosfataza (BLAP) određena je u serumu hemilumiiscentnom imuno metodom. Faktor rasta fibroblasta 23 (FGF23) u serumu određen je enzimskom imunosorbetnom metodom. Nivoi 25-hidroksivitamina D (25(OH)D), intaktnog paratiroidnog hormona (iPTH) i betakros-lapsa (CTX) izmereni su elektrohemiluminiscentnom DEXA tehnologijom (dual-energy x-ray apsorpciometrijom) kako bi se procenila BMD.

          Rezultati

          Nađena je značajno negativna statistička korelacija BALP nivoa i ukupnog telesnog BMD (r= -0,268: P = 0,015) u femoralnom delu vrata (FN) (r = -0,219; P = 0,037). BALP je bila u negativnoj korelaciji sa ukupnom BMD naročito kod FN pacijenata sa BMI < 30, FGF23 koncentracije su bile takođe u negativnoj korelaciji sa BMD u lumbalnom delu (LS) (r = -0,209, P = 0,046). Kod osteopeničnih pacijenata nađene je inverzna korelacija između 25(OH)D koncentracije i DMD u LS polažaju (r = -0,336; P = 0,038). U grupi muških osoba nađena je negativna korelacija između iPTH i ukupnog BMD (r = -0,326; P = 0,015). Međutim, nađena je pozitivna korelacija između ekspresije kalcijuma i BMD u LS (r = 0,270: P = 0,031).

          Zaključak

          FGF23 i BALP mogu da predvide gubitak kosti kod ESRD preko izrazite korelacije sa BMD u LS i FN položajima.

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          Most cited references38

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          Consensus development conference: diagnosis, prophylaxis, and treatment of osteoporosis.

          (1993)
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            Loss of DMP1 causes rickets and osteomalacia and identifies a role for osteocytes in mineral metabolism.

            The osteocyte, a terminally differentiated cell comprising 90%-95% of all bone cells, may have multiple functions, including acting as a mechanosensor in bone (re)modeling. Dentin matrix protein 1 (encoded by DMP1) is highly expressed in osteocytes and, when deleted in mice, results in a hypomineralized bone phenotype. We investigated the potential for this gene not only to direct skeletal mineralization but also to regulate phosphate (P(i)) homeostasis. Both Dmp1-null mice and individuals with a newly identified disorder, autosomal recessive hypophosphatemic rickets, manifest rickets and osteomalacia with isolated renal phosphate-wasting associated with elevated fibroblast growth factor 23 (FGF23) levels and normocalciuria. Mutational analyses showed that autosomal recessive hypophosphatemic rickets family carried a mutation affecting the DMP1 start codon, and a second family carried a 7-bp deletion disrupting the highly conserved DMP1 C terminus. Mechanistic studies using Dmp1-null mice demonstrated that absence of DMP1 results in defective osteocyte maturation and increased FGF23 expression, leading to pathological changes in bone mineralization. Our findings suggest a bone-renal axis that is central to guiding proper mineral metabolism.
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              Pathogenic role of Fgf23 in Hyp mice.

              Inactivating mutations of the PHEX (phosphate-regulating gene with homologies to endopeptidases on the X chromosome) endopeptidase, the disease-causing gene in X-linked hypophosphatemia (XLH), results in increased circulating levels of fibroblastic growth factor-23 (FGF23), a bone-derived phosphaturic factor. To determine the causal role of FGF23 in XLH, we generated a combined Fgf23-deficient enhanced green fluorescent protein (eGFP) reporter and Phex-deficient Hyp mouse model (Fgf23(+/-)/Hyp). eGFP expression was expressed in osteocytes embedded in bone that exhibited marked upregulation of eGFP in response to Phex deficiency and in CD31-positive cells in bone marrow venules that expressed low eGFP levels independently of Phex. In bone marrow stromal cells (BMSCs) derived from Fgf23(-/-)/Hyp mice, eGFP expression was also selectively increased in osteocyte-like cells within mineralization nodules and detected in low levels in CD31-positive cells. Surprisingly, eGFP expression was not increased in cell surface osteoblasts, indicating that Phex deficiency is necessary but not sufficient for increased Fgf23 expression in the osteoblast lineage. Additional factors, associated with either osteocyte differentiation and/or extracellular matrix, are necessary for Phex deficiency to stimulate Fgf23 gene transcription in bone. Regardless, the deletion of Fgf23 from Hyp mice reversed the hypophosphatemia, abnormal 1,25(OH)(2)D(3) levels, rickets, and osteomalacia associated with Phex deficiency. These results suggest that Fgf23 acts downstream of Phex to cause both the renal and bone phenotypes in Hyp mice.
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                Author and article information

                Journal
                J Med Biochem
                J Med Biochem
                jomb
                jomb
                Journal of Medical Biochemistry
                Sciendo
                1452-8258
                1452-8266
                October 2019
                30 July 2019
                : 38
                : 4
                : 418-426
                Affiliations
                [1 ]Immuno-Rheumatology Research Laboratory, Rheumatology Department, La Rabta Hospital, University of Tunis-El Manar , Tunis, Tunisia
                [2 ]Laboratory of Clinical Biochemistry and Hormonology; Pasteur Institute of Tunis, University of Tunis-El Manar , Tunis, Tunisia
                [3 ]Department of Basic Sciences, Medicine School of Tunis, University of Tunis-El Manar , Tunis, Tunisia
                [4 ]Nephrology Department, La Rabta Hospital, Medicine School of Tunis, University of Tunis-El Manar , Tunis, Tunisia
                [5 ]Rheumatology Department, La Rabta Hospital, Medicine School of Tunis, University of Tunis-El Manar , Tunis, Tunisia
                Author notes
                [* ] Address: 13; Pasteur place, B.P. 74; 1002 Tunis, Belvedere, Tunisia, Phone number: +216 95 361 654 manou.bouk@ 123456live.fr
                Article
                jomb-2019-0002
                10.2478/jomb-2019-0002
                6708290
                31496905
                1bda3b45-1270-46af-9419-28bb61bd76fd
                © 2019 Mouna Bouksila, Mehdi Mrad, Wajih Kaabachi, Eya Kalai, Wided Smaoui, Sonia Rekik, Asma Krir, Nesrine Issaoui, Kamel Hamzaoui, Hela Sahli, Elhem Cheour El Kateb, Mohammed Karim Zouaghi, Afef Bahlous, published by Sciendo

                This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.

                History
                : 20 November 2018
                : 04 January 2019
                Page count
                Pages: 9
                Categories
                Original Paper

                25-hydroxyvitamin d,bone alkaline phosphatase,bone mineral density,bone mineral disorder,chronic kidney disease,fibroblast growth factor 23

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