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      The Emerging Role of Nutritional Vitamin D in Secondary Hyperparathyroidism in CKD

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          Abstract

          In chronic kidney disease (CKD), hyperphosphatemia induces fibroblast growth factor-23 (FGF-23) expression that disturbs renal 1,25-dihydroxy vitamin D (1,25D) synthesis; thereby increasing parathyroid hormone (PTH) production. FGF-23 acts on the parathyroid gland (PTG) to increase 1α-hydroxylase activity and results in increase intra-gland 1,25D production that attenuates PTH secretion efficiently if sufficient 25D are available. Interesting, calcimimetics can further increase PTG 1α-hydroxylase activity that emphasizes the demand for nutritional vitamin D (NVD) under high PTH status. In addition, the changes in hydroxylase enzyme activity highlight the greater parathyroid 25-hydroxyvitmain D (25D) requirement in secondary hyperparathyroidism (SHPT); the higher proportion of oxyphil cells as hyperplastic parathyroid progression; lower cytosolic vitamin D binding protein (DBP) content in the oxyphil cell; and calcitriol promote vitamin D degradation are all possible reasons supports nutritional vitamin D (NVD; e.g., Cholecalciferol) supplement is crucial in SHPT. Clinically, NVD can effectively restore serum 25D concentration and prevent the further increase in PTH level. Therefore, NVD might have the benefit of alleviating the development of SHPT in early CKD and further lowering PTH in moderate to severe SHPT in dialysis patients.

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          Most cited references107

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          Distribution of the vitamin D receptor and 1 alpha-hydroxylase in human brain.

          Despite a growing body of evidence that Vitamin D is involved in mammalian brain functioning, there has been a lack of direct evidence about its role in the human brain. This paper reports, for the first time, the distribution of the 1,25-dihydroxyvitamin D3 receptor (VDR), and 1alpha-hydroxylase (1alpha-OHase), the enzyme responsible for the formation of the active vitamin in the human brain. The receptor and the enzyme were found in both neurons and glial cells in a regional and layer-specific pattern. The VDR was restricted to the nucleus whilst 1alpha-OHase was distributed throughout the cytoplasm. The distribution of the VDR in human brain was strikingly similar to that reported in rodents. Many regions contained equivalent amounts of both the VDR and 1alpha-OHase, however the macrocellular cells within the nucleus basalis of Meynert (NBM) and the Purkinje cells in the cerebellum expressed 1alpha-OHase in the absence of VDR. The strongest immunohistochemical staining for both the receptor and enzyme was in the hypothalamus and in the large (presumably dopaminergic) neurons within the substantia nigra. The observed distribution of the VDR is consistent with the proposal that Vitamin D operates in a similar fashion to the known neurosteroids. The widespread distribution of 1alpha-OHase and the VDR suggests that Vitamin D may have autocrine/paracrine properties in the human brain.
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            The parathyroid is a target organ for FGF23 in rats.

            Phosphate homeostasis is maintained by a counterbalance between efflux from the kidney and influx from intestine and bone. FGF23 is a bone-derived phosphaturic hormone that acts on the kidney to increase phosphate excretion and suppress biosynthesis of vitamin D. FGF23 signals with highest efficacy through several FGF receptors (FGFRs) bound by the transmembrane protein Klotho as a coreceptor. Since most tissues express FGFR, expression of Klotho determines FGF23 target organs. Here we identify the parathyroid as a target organ for FGF23 in rats. We show that the parathyroid gland expressed Klotho and 2 FGFRs. The administration of recombinant FGF23 led to an increase in parathyroid Klotho levels. In addition, FGF23 activated the MAPK pathway in the parathyroid through ERK1/2 phosphorylation and increased early growth response 1 mRNA levels. Using both rats and in vitro rat parathyroid cultures, we show that FGF23 suppressed both parathyroid hormone (PTH) secretion and PTH gene expression. The FGF23-induced decrease in PTH secretion was prevented by a MAPK inhibitor. These data indicate that FGF23 acts directly on the parathyroid through the MAPK pathway to decrease serum PTH. This bone-parathyroid endocrine axis adds a new dimension to the understanding of mineral homeostasis.
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              Vitamin D levels and early mortality among incident hemodialysis patients.

              Vitamin D deficiency is associated with cardiovascular disease, the most common cause of mortality in hemodialysis patients. To investigate the relation between blood levels of 25-hydroxyvitamin D (25D) and 1,25-dihydroxyvitamin D (1,25D) with hemodialysis outcomes, we measured baseline vitamin D levels in a cross-sectional analysis of 825 consecutive patients from within a prospective cohort of incident US hemodialysis patients. Of these patients, 78% were considered vitamin D deficient with 18% considered severely deficient. Calcium, phosphorus, and parathyroid hormone levels correlated poorly with 25D and 1,25D concentrations. To test the association between baseline vitamin D levels and 90-day mortality, we selected the next 175 consecutive participants who died within 90 days and compared them to the 750 patients who survived in a nested case-control analysis. While low vitamin D levels were associated with increased mortality, significant interaction was noted between vitamin D levels, subsequent active vitamin D therapy, and survival. Compared to patients with the highest 25D or 1,25D levels who received therapy, untreated deficient patients were at significantly increased risk for early mortality. Our study shows that among incident hemodialysis patients, vitamin D deficiency is common, correlates poorly with other components of mineral metabolism and is associated with increased early mortality.
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                Author and article information

                Journal
                Nutrients
                Nutrients
                nutrients
                Nutrients
                MDPI
                2072-6643
                03 December 2018
                December 2018
                : 10
                : 12
                : 1890
                Affiliations
                [1 ]Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan; janlin0123@ 123456gmail.com (C.-L.L.); athletics910@ 123456gmail.com (Y.-C.H.); wayneliu55@ 123456gmail.com (W.-C.L.); 11044@ 123456s.tmu.edu.tw (C.-M.Z.); linyf@ 123456shh.org.tw (Y.-F.L.); shyujeff@ 123456mail.ndmctsgh.edu.tw (J.-F.S.)
                [2 ]Division of Nephrology, Department of Medicine, Fu Jen Catholic University Hospital, School of Medicine, Fu Jen Catholic University, New Taipei City 242, Taiwan; 039666@ 123456mail.fju.edu.tw (G.-M.J.); roy_lii@ 123456yahoo.com.tw (Z.-Y.L.)
                [3 ]Division of Cardiology, Department of Medicine, Fu Jen Catholic University Hospital, School of Medicine, Fu Jen Catholic University, New Taipei City 242, Taiwan; ocean0829@ 123456yahoo.com
                [4 ]Division of Nephrology, Department of Medicine, Cardinal-Tien Hospital, School of Medicine, Fu Jen Catholic University, New Taipei City 23155, Taiwan
                [5 ]Division of Nephrology, Department of Internal Medicine, Tungs’ Taichung MetroHarbor Hospital, Taichung City 433, Taiwan
                [6 ]Division of Nephrology, Department of Internal Medicine, Shuang Ho Hospital, New Taipei City 235, Taiwan
                [7 ]Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei 11103, Taiwan
                [8 ]Department of Biology and Anatomy, National Defense Medical Center, Taipei 114, Taiwan
                [9 ]Kidney Dialysis Center, Kamifukuoka General Hospital, Saitama 356, Japan; remyneko@ 123456yahoo.co.jp
                [10 ]Department of Medicine, Show-Chwan Memorial Hospital, Changhua 50008, Taiwan; c_y_huang_alex@ 123456yahoo.com.tw
                Author notes
                [* ]Correspondence: kuochenglu@ 123456gmail.com
                Author information
                https://orcid.org/0000-0002-9452-5179
                https://orcid.org/0000-0003-0370-3951
                https://orcid.org/0000-0001-7861-5054
                Article
                nutrients-10-01890
                10.3390/nu10121890
                6316278
                30513912
                9ae760e0-a837-4ff1-89b7-375e10e3d2a4
                © 2018 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 13 September 2018
                : 23 November 2018
                Categories
                Review

                Nutrition & Dietetics
                calcitriol,calcimimetics,nutritional vitamin d,secondary hyperparathyroidism

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