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      New Aspects of the Kidney in the Regulation of Fibroblast Growth Factor 23 (FGF23) and Mineral Homeostasis

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          Abstract

          The bone-derived hormone fibroblast growth factor 23 (FGF23) acts in concert with parathyroid hormone (PTH) and the active vitamin D metabolite calcitriol in the regulation of calcium (Ca) and phosphate (P) homeostasis. More factors are being identified to regulate FGF23 levels and the endocrine loops between the three hormones. The present review summarizes the complex regulation of FGF23 and the disturbed FGF23/Klotho system in chronic kidney disease (CKD). In addition to the reduced ability of the injured kidney to regulate plasma levels of FGF23, several CKD-related factors have been shown to stimulate FGF23 production. The high circulating FGF23 levels have detrimental effects on erythropoiesis, the cardio-vascular system and the immune system, all contributing to the disturbed system biology in CKD. Moreover, new factors secreted by the injured kidney and the uremic calcified vasculature play a role in the mineral and bone disorder in CKD and create a vicious pathological crosstalk.

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          Mutation of the mouse klotho gene leads to a syndrome resembling ageing.

          M Kuro-O, Y Matsumura, H Aizawa … (1997)
          A new gene, termed klotho, has been identified that is involved in the suppression of several ageing phenotypes. A defect in klotho gene expression in the mouse results in a syndrome that resembles human ageing, including a short lifespan, infertility, arteriosclerosis, skin atrophy, osteoporosis and emphysema. The gene encodes a membrane protein that shares sequence similarity with the beta-glucosidase enzymes. The klotho gene product may function as part of a signalling pathway that regulates ageing in vivo and morbidity in age-related diseases.
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            Fibroblast growth factor 23 is elevated before parathyroid hormone and phosphate in chronic kidney disease.

            Tamara Isakova, Patricia Wahl, Gabriela S. Vargas … (2011)
            Fibroblast growth factor 23 (FGF23) regulates phosphorus metabolism and is a strong predictor of mortality in dialysis patients. FGF23 is thought to be an early biomarker of disordered phosphorus metabolism in the initial stages of chronic kidney disease (CKD). We measured FGF23 in baseline samples from 3879 patients in the Chronic Renal Insufficiency Cohort study, which is a diverse cohort of patients with CKD stage 2-4. Mean serum phosphate and median parathyroid hormone (PTH) levels were in the normal range, but median FGF23 was markedly greater than in healthy populations, and increased significantly with decreasing estimated glomerular filtration rate (eGFR). High levels of FGF23, defined as being above 100 RU/ml, were more common than secondary hyperparathyroidism and hyperphosphatemia in all strata of eGFR. The threshold of eGFR at which the slope of FGF23 increased was significantly higher than the corresponding threshold for PTH based on non-overlapping 95% confidence intervals. Thus, increased FGF23 is a common manifestation of CKD that develops earlier than increased phosphate or PTH. Hence, FGF23 measurements may be a sensitive early biomarker of disordered phosphorus metabolism in patients with CKD and normal serum phosphate levels.
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              Coordination of circadian timing in mammals.

              Steven Reppert, David Weaver (2002)
              Time in the biological sense is measured by cycles that range from milliseconds to years. Circadian rhythms, which measure time on a scale of 24 h, are generated by one of the most ubiquitous and well-studied timing systems. At the core of this timing mechanism is an intricate molecular mechanism that ticks away in many different tissues throughout the body. However, these independent rhythms are tamed by a master clock in the brain, which coordinates tissue-specific rhythms according to light input it receives from the outside world.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 20 November 2020
                Publication date Collection: November 2020
                Volume: 21
                Issue: 22
                Electronic Location Identifier: 8810
                Affiliations
                [1 ]Department of Nephrology, Rigshospitalet, University of Copenhagen, 2100 Copenhagen, Denmark; Klaus.oelgaard@ 123456regionh.dk (K.O.); Ewa.lewin@ 123456regionh.dk (E.L.)
                [2 ]Department of Nephrology, Herlev Hospital, University of Copenhagen, 2730 Herlev, Denmark
                Author notes
                Article
                Publisher ID: ijms-21-08810
                DOI: 10.3390/ijms21228810
                PMC ID: 7699902
                PubMed ID: 33233840
                SO-VID: 672ffbdf-6016-44a2-9f7d-13fcdacf0019
                Copyright © © 2020 by the authors.
                License:

                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
                Date received : 28 October 2020
                Date accepted : 19 November 2020
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: acute kidney failure,chronic kidney failure,calcium,phosphate,klotho,pth,calcitriol,activin a,ckd-mbd,circadian rhythm,bone,crosstalk
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: acute kidney failure, chronic kidney failure, calcium, phosphate, klotho, pth, calcitriol, activin a, ckd-mbd, circadian rhythm, bone, crosstalk

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