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Enhanced induction of Cyp24a1 by FGF23 but low serum 24,25-dihydroxyvitamin D in CKD: implications for therapy
Adriana S Dusso1, Mariano Rodriguez
1Experimental Nephrology Laboratory, IRBLleida (Lleida Institute for Biomedical Research), Lleida School of Medicine, Universidad de Lleida, Lleida, Spain. adusso@irblleida.cat
Abstract:
In normal people, induction by FGF23 of renal Cyp24a1, the enzyme that degrades 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, helps to protect from the disorders caused by excessive 1,25-dihydroxyvitamin D. Dai and co-workers report, however, that in human and mouse kidney disease, high FGF23 concurs with low rather than high serum 24,25-dihydroxyvitamin D, a biomarker of Cyp24a1 activity. Their characterization of the underlying mechanisms provides new understanding of how kidney disease impairs the health benefits of vitamin D-FGF23/klotho interactions.
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