Fibroblast growth factor 23: uremic toxin or innocent bystander in chronic kidney disease?
Our understanding of the role of FGF23 in CKD continues to rapidly advance. Information regarding the onset of FGF23 elevations in relationship to changes in parathyroid gland function, renal production of 1,25(OH)2D, and phosphate excretion may provide clues to its role in the adaptive changes in mineral homeostasis that occur during progressive kidney diseases. More knowledge of the regulation and function of FGF23 in CKD will likely improve our understanding of the pathogenesis of disordered mineral metabolism, lead to changes in the medical management of this disorder, and establish additional biological links between disorders of mineral metabolism and associated comorbidities in patients with progressive renal failure.
Stubbs
Jason R
JR
Division of Nephrology and Hypertension, University of Kansas Medical Center, Kansas City, KS, USA.
Quarles
L Darryl
LD
D002117:Calcitriol / Q000502:physiology; D002318:Cardiovascular Diseases / Q000209:etiology; D003072:Cognition Disorders / Q000209:etiology; D015897:Comorbidity; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000502:physiology*; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000209:etiology; D007676:Kidney Failure, Chronic / Q000150:complications* / Q000378:metabolism*; D012307:Risk Factors; D015854:Up-Regulation / Q000502:physiology
C000717427:FGF23 protein, human; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23; D002117:Calcitriol