title: Enigmatic Cassandra: renal FGF23 formation in polycystic kidney disease.
abstract: Fibroblast growth factor 23 (FGF23) counteracts phosphate excess and tissue calcification. Phosphate intake, Ca(2+), parathyroid hormone, and 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) stimulate FGF23 release from bone. FGF23 inhibits renal 1,25(OH)2D3 formation and phosphate reabsorption. Spichtig and colleagues demonstrate that FGF23 is generated in rodent polycystic kidneys, leading to an increase in plasma FGF23 concentration before reduction in kidney function. FGF23 fails to appreciably downregulate renal phosphate transporter and 1α-25OH-vitamin D hydroxylase activities. Unraveling underlying mechanisms may open diagnostic and therapeutic opportunities.
authors.affiliation: Department of Physiology, University of Tübingen, Tübingen, Germany.
authors.forename: Florian
authors.initials: F
authors.lastname: Lang
authors.affiliation: Department of Physiology, University of Tübingen, Tübingen, Germany.
authors.forename: Michael
authors.initials: M
authors.lastname: Föller
mesh_terms: D000818:Animals; D005260:Female; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism*; D008297:Male; D007690:Polycystic Kidney Diseases / Q000378:metabolism*
chemical_list: C505605:Fgf23 protein, rat; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23