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Fibroblast growth factor-23 in early chronic kidney disease: additional support in favor of a phosphate-centric paradigm for the pathogenesis of secondary hyperparathyroidism.
Clin J Am Soc Nephrol. 2010 Jul; 5(7):1268-76.CJ

Abstract

BACKGROUND AND OBJECTIVES

The discovery of fibroblast growth factor-23 (FGF-23) and the elucidation of its function as a phosphaturic and 1,25(OH)2VitD counter-regulatory hormone provides a new conceptual framework for the understanding of the pathogenesis of secondary hyperparathyroidism. This study aims to elucidate the complex associations between FGF-23, parathyroid hormone (PTH), 1,25(OH)2D, and phosphate in patients with early-stage chronic kidney disease (CKD) and to provide clinical evidence in favor of the new phosphate-centric paradigm for the pathogenesis of secondary hyperparathyroidism.

DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS

Serum biointact PTH and FGF-23, 25(OH)D, 1,25(OH)2D, calcium, phosphate, 24-hour urine excretion of phosphate and calcium, and urinary fractional excretion of phosphate were determined in a cross-sectional study including 125 patients with CKD stages 1 to 3.

RESULTS

Serum phosphate levels showed an inverse association with estimated GFR (eGFR), but were within the normal range in all but one patient. FGF-23 and PTH were inversely associated with eGFR, even in the subgroup of patients with CKD stages 1 and 2. High FGF-23 levels were significantly more prevalent than high PTH levels. The urinary fractional excretion of phosphate was highest in patients with both a high serum FGF-23 and PTH level. Increased FGF-23 and phosphate and decreased 25(OH)D were independently associated with decreased 1,25(OH)2D.

CONCLUSIONS

Our data are in favor of the new paradigm for the pathogenesis of secondary hyperparathyroidism according to which a reduced phosphate excretion capacity is the principal abnormality that initiates secondary hyperparathyroidism.

Authors+Show Affiliations

Department of Medicine, University Hos;pital Leuven, Leuven, Belgium. Pieter.Evenepoel@uz.kuleuven.ac.beNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

20448073

Citation

Evenepoel, Pieter, et al. "Fibroblast Growth Factor-23 in Early Chronic Kidney Disease: Additional Support in Favor of a Phosphate-centric Paradigm for the Pathogenesis of Secondary Hyperparathyroidism." Clinical Journal of the American Society of Nephrology : CJASN, vol. 5, no. 7, 2010, pp. 1268-76.
Evenepoel P, Meijers B, Viaene L, et al. Fibroblast growth factor-23 in early chronic kidney disease: additional support in favor of a phosphate-centric paradigm for the pathogenesis of secondary hyperparathyroidism. Clin J Am Soc Nephrol. 2010;5(7):1268-76.
Evenepoel, P., Meijers, B., Viaene, L., Bammens, B., Claes, K., Kuypers, D., Vanderschueren, D., & Vanrenterghem, Y. (2010). Fibroblast growth factor-23 in early chronic kidney disease: additional support in favor of a phosphate-centric paradigm for the pathogenesis of secondary hyperparathyroidism. Clinical Journal of the American Society of Nephrology : CJASN, 5(7), 1268-76. https://doi.org/10.2215/CJN.08241109
Evenepoel P, et al. Fibroblast Growth Factor-23 in Early Chronic Kidney Disease: Additional Support in Favor of a Phosphate-centric Paradigm for the Pathogenesis of Secondary Hyperparathyroidism. Clin J Am Soc Nephrol. 2010;5(7):1268-76. PubMed PMID: 20448073.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fibroblast growth factor-23 in early chronic kidney disease: additional support in favor of a phosphate-centric paradigm for the pathogenesis of secondary hyperparathyroidism. AU - Evenepoel,Pieter, AU - Meijers,Björn, AU - Viaene,Liesbeth, AU - Bammens,Bert, AU - Claes,Kathleen, AU - Kuypers,Dirk, AU - Vanderschueren,Dirk, AU - Vanrenterghem,Yves, Y1 - 2010/05/06/ PY - 2010/5/8/entrez PY - 2010/5/8/pubmed PY - 2010/10/27/medline SP - 1268 EP - 76 JF - Clinical journal of the American Society of Nephrology : CJASN JO - Clin J Am Soc Nephrol VL - 5 IS - 7 N2 - BACKGROUND AND OBJECTIVES: The discovery of fibroblast growth factor-23 (FGF-23) and the elucidation of its function as a phosphaturic and 1,25(OH)2VitD counter-regulatory hormone provides a new conceptual framework for the understanding of the pathogenesis of secondary hyperparathyroidism. This study aims to elucidate the complex associations between FGF-23, parathyroid hormone (PTH), 1,25(OH)2D, and phosphate in patients with early-stage chronic kidney disease (CKD) and to provide clinical evidence in favor of the new phosphate-centric paradigm for the pathogenesis of secondary hyperparathyroidism. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Serum biointact PTH and FGF-23, 25(OH)D, 1,25(OH)2D, calcium, phosphate, 24-hour urine excretion of phosphate and calcium, and urinary fractional excretion of phosphate were determined in a cross-sectional study including 125 patients with CKD stages 1 to 3. RESULTS: Serum phosphate levels showed an inverse association with estimated GFR (eGFR), but were within the normal range in all but one patient. FGF-23 and PTH were inversely associated with eGFR, even in the subgroup of patients with CKD stages 1 and 2. High FGF-23 levels were significantly more prevalent than high PTH levels. The urinary fractional excretion of phosphate was highest in patients with both a high serum FGF-23 and PTH level. Increased FGF-23 and phosphate and decreased 25(OH)D were independently associated with decreased 1,25(OH)2D. CONCLUSIONS: Our data are in favor of the new paradigm for the pathogenesis of secondary hyperparathyroidism according to which a reduced phosphate excretion capacity is the principal abnormality that initiates secondary hyperparathyroidism. SN - 1555-905X UR - https://www.unboundmedicine.com/medline/citation/20448073/Fibroblast_growth_factor_23_in_early_chronic_kidney_disease:_additional_support_in_favor_of_a_phosphate_centric_paradigm_for_the_pathogenesis_of_secondary_hyperparathyroidism_ L2 - https://cjasn.asnjournals.org/cgi/pmidlookup?view=long&pmid=20448073 DB - PRIME DP - Unbound Medicine ER -