LAS VEGAS—Fibroblast growth factor 23 (FGF-23) is not significantly associated with dietary phosphorus or urinary phosphorus excretion, researchers reported at the National Kidney Foundation’s Spring Clinical Meetings.
The finding, by Jessica Houston, MD, and collaborators at the University of Miami Miller School of Medicine, suggests that additional factors may mediate the increase in FGF-23 in patients with chronic kidney disease (CKD), investigators concluded.
FGF-23 is a central regulator of phosphorus metabolism that may serve as a novel prognostic indicator of vascular disease risk, Dr. Houston’s team noted in a poster. Although dietary phosphorus has been shown to modulate FGF-23 secretion in health individuals, the association of diet with FGF-23 in CKD has been studied in less detail, they observed.
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The investigators evaluated cross-sectional associations of FGF-23 with estimated dietary phosphorus intake, 24-hour urinary phosphate, and augmentation index (AI), a validated
measure of vascular stiffness) in 74 CKD patients with mean creatinine clearance of 51 mL/min. “Serum phosphate varied little with worsening renal function,” they stated. However, average daily phosphorus intake and 24-hour urinary phosphate excretion decreased substantially from the highest to the lowest quartile of creatinine clearance (by 44% and 62%, respectively), they reported. Dietary phosphorus was not associated with AI.
Additional studies are needed to determine the primary mediators of increased FGF-23 levels in CKD and to further assess the association of FGF23 with subclinical markers
of vascular disease, they wrote.
