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Fibroblast growth factor 23 and markers of mineral metabolism in individuals with preserved renal function.
Kidney Int. 2016 09; 90(3):648-57.KI

Abstract

Fibroblast growth factor 23 (FGF23) is a bone-derived hormone that regulates phosphate homeostasis. Circulating FGF23 is elevated in chronic kidney disease (CKD) and independently associated with poor renal and cardiovascular outcomes and mortality. Because the study of FGF23 in individuals with normal renal function has received little attention, we examined in a large, population-based study of 1128 participants the associations of FGF23 with markers of mineral metabolism and renal function. The median estimated glomerular filtration rate (eGFR) of the cohort was 105 ml/min per 1.73 m(2), and the median plasma FGF23 was 78.5 RU/ml. FGF23 increased and plasma 1,25-dihydroxyvitamin D3 decreased significantly below an eGFR threshold of 102 and 99 ml/min per 1.73 m(2), respectively. In contrast, plasma parathyroid hormone increased continuously with decreasing eGFR and was first significantly elevated at an eGFR of 126 ml/min per 1.73 m(2). On multivariable analysis adjusting for sex, age, body mass index, and GFR, FGF23 was negatively associated with 1,25-dihydroxyvitamin D3, and urinary absolute and fractional calcium excretion but not with serum calcium or parathyroid hormone. We found a positive association of FGF23 with plasma phosphate, but no association with urinary absolute or fractional phosphate excretion and, unexpectedly, a positive association with tubular maximum phosphate reabsorption/GFR. Thus, in the absence of CKD, parathyroid hormone increases earlier than FGF23 when the eGFR decreases. The increase in FGF23 occurs at a higher eGFR threshold than previously reported and is closely associated with a decrease in 1,25-dihydroxyvitamin D3. We speculate that the main demonstrable effect of FGF23 in the setting of preserved renal function is suppression of 1,25-dihydroxyvitamin D3 rather than stimulation of renal phosphate excretion.

Authors+Show Affiliations

Department of Nephrology, Hypertension, and Clinical Pharmacology, Bern University Hospital, University of Bern, Bern, Switzerland; Institute of Biochemistry and Molecular Medicine, University of Bern, Bern, Switzerland; Department of Clinical Research, University of Bern, Bern, Switzerland.Department of Nephrology, Hypertension, and Clinical Pharmacology, Bern University Hospital, University of Bern, Bern, Switzerland; Department of Clinical Research, University of Bern, Bern, Switzerland.Nephrology Service, University Hospital of Lausanne, Lausanne, Switzerland.Nephrology Service, Department of Specialties of Internal Medicine, University Hospital of Geneva, Geneva, Switzerland.Cardiology Service, Department of Specialties of Internal Medicine, University Hospital of Geneva, Geneva, Switzerland.Department of Community Medicine, Primary Care and Emergency Medicine, University Hospital of Geneva, Geneva, Switzerland; Institute of Social and Preventive Medicine, University Hospital of Lausanne, Lausanne, Switzerland.Department of Laboratory Medicine, Bern University Hospital, University of Bern, Bern, Switzerland; Department of Clinical Research, University of Bern, Bern, Switzerland.Institute of Social and Preventive Medicine, University Hospital of Lausanne, Lausanne, Switzerland.Department of Nephrology, Hypertension, and Clinical Pharmacology, Bern University Hospital, University of Bern, Bern, Switzerland.Department of Laboratory Medicine, Bern University Hospital, University of Bern, Bern, Switzerland; Department of Clinical Research, University of Bern, Bern, Switzerland.Institute of Physiology, University of Zurich, Zurich, Switzerland.Endocrinology Service, Department of Internal Medicine Specialties, University Hospital of Geneva, Geneva, Switzerland.Nephrology Service, University Hospital of Lausanne, Lausanne, Switzerland; Department of Clinical Research, University of Bern, Bern, Switzerland.Nephrology Service, Department of Specialties of Internal Medicine, University Hospital of Geneva, Geneva, Switzerland.Institute of Social and Preventive Medicine, University Hospital of Lausanne, Lausanne, Switzerland.Department of Nephrology, Hypertension, and Clinical Pharmacology, Bern University Hospital, University of Bern, Bern, Switzerland; Department of Clinical Research, University of Bern, Bern, Switzerland.Department of Nephrology, Hypertension, and Clinical Pharmacology, Bern University Hospital, University of Bern, Bern, Switzerland; Institute of Biochemistry and Molecular Medicine, University of Bern, Bern, Switzerland; Department of Clinical Research, University of Bern, Bern, Switzerland. Electronic address: Daniel.Fuster@ibmm.unibe.ch.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27370409

Citation

Dhayat, Nasser A., et al. "Fibroblast Growth Factor 23 and Markers of Mineral Metabolism in Individuals With Preserved Renal Function." Kidney International, vol. 90, no. 3, 2016, pp. 648-57.
Dhayat NA, Ackermann D, Pruijm M, et al. Fibroblast growth factor 23 and markers of mineral metabolism in individuals with preserved renal function. Kidney Int. 2016;90(3):648-57.
Dhayat, N. A., Ackermann, D., Pruijm, M., Ponte, B., Ehret, G., Guessous, I., Leichtle, A. B., Paccaud, F., Mohaupt, M., Fiedler, G. M., Devuyst, O., Pechère-Bertschi, A., Burnier, M., Martin, P. Y., Bochud, M., Vogt, B., & Fuster, D. G. (2016). Fibroblast growth factor 23 and markers of mineral metabolism in individuals with preserved renal function. Kidney International, 90(3), 648-57. https://doi.org/10.1016/j.kint.2016.04.024
Dhayat NA, et al. Fibroblast Growth Factor 23 and Markers of Mineral Metabolism in Individuals With Preserved Renal Function. Kidney Int. 2016;90(3):648-57. PubMed PMID: 27370409.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fibroblast growth factor 23 and markers of mineral metabolism in individuals with preserved renal function. AU - Dhayat,Nasser A, AU - Ackermann,Daniel, AU - Pruijm,Menno, AU - Ponte,Belen, AU - Ehret,Georg, AU - Guessous,Idris, AU - Leichtle,Alexander Benedikt, AU - Paccaud,Fred, AU - Mohaupt,Markus, AU - Fiedler,Georg-Martin, AU - Devuyst,Olivier, AU - Pechère-Bertschi,Antoinette, AU - Burnier,Michel, AU - Martin,Pierre-Yves, AU - Bochud,Murielle, AU - Vogt,Bruno, AU - Fuster,Daniel G, Y1 - 2016/06/28/ PY - 2015/12/30/received PY - 2016/04/21/revised PY - 2016/04/28/accepted PY - 2016/7/3/entrez PY - 2016/7/3/pubmed PY - 2017/10/17/medline KW - FGF23 KW - PTH KW - TmP/GFR KW - calcium KW - phosphate SP - 648 EP - 57 JF - Kidney international JO - Kidney Int VL - 90 IS - 3 N2 - Fibroblast growth factor 23 (FGF23) is a bone-derived hormone that regulates phosphate homeostasis. Circulating FGF23 is elevated in chronic kidney disease (CKD) and independently associated with poor renal and cardiovascular outcomes and mortality. Because the study of FGF23 in individuals with normal renal function has received little attention, we examined in a large, population-based study of 1128 participants the associations of FGF23 with markers of mineral metabolism and renal function. The median estimated glomerular filtration rate (eGFR) of the cohort was 105 ml/min per 1.73 m(2), and the median plasma FGF23 was 78.5 RU/ml. FGF23 increased and plasma 1,25-dihydroxyvitamin D3 decreased significantly below an eGFR threshold of 102 and 99 ml/min per 1.73 m(2), respectively. In contrast, plasma parathyroid hormone increased continuously with decreasing eGFR and was first significantly elevated at an eGFR of 126 ml/min per 1.73 m(2). On multivariable analysis adjusting for sex, age, body mass index, and GFR, FGF23 was negatively associated with 1,25-dihydroxyvitamin D3, and urinary absolute and fractional calcium excretion but not with serum calcium or parathyroid hormone. We found a positive association of FGF23 with plasma phosphate, but no association with urinary absolute or fractional phosphate excretion and, unexpectedly, a positive association with tubular maximum phosphate reabsorption/GFR. Thus, in the absence of CKD, parathyroid hormone increases earlier than FGF23 when the eGFR decreases. The increase in FGF23 occurs at a higher eGFR threshold than previously reported and is closely associated with a decrease in 1,25-dihydroxyvitamin D3. We speculate that the main demonstrable effect of FGF23 in the setting of preserved renal function is suppression of 1,25-dihydroxyvitamin D3 rather than stimulation of renal phosphate excretion. SN - 1523-1755 UR - https://www.unboundmedicine.com/medline/citation/27370409/Fibroblast_growth_factor_23_and_markers_of_mineral_metabolism_in_individuals_with_preserved_renal_function_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0085-2538(16)30200-9 DB - PRIME DP - Unbound Medicine ER -