Title: Fibroblast Growth Factor-23 in Early Chronic Kidney Disease: Additional Support in Favor of a Phosphate-Centric Paradigm for the Pathogenesis of Secondary Hyperparathyroidism
Authors: Evenepoel, Pieter ×
Meijers, Björn
Viaene, Liesbeth
Bammens, Bert
Claes, Kathleen
Kuypers, Dirk
Vanderschueren, Dirk
Vanrenterghem, Yves #
Issue Date: May-2010
Publisher: American Society of Nephrology
Series Title: Clinical Journal of the American Society of Nephrology vol:5 issue:7 pages:1268-1276
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)(2)VitD 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)(2)D, 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)(2)D, 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)(2)D. 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.
ISSN: 1555-9041
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Clinical and Experimental Endocrinology
Laboratory of Nephrology
× corresponding author
# (joint) last author

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