ArticleKidney international2012
Assessment of 24,25(OH)2D levels does not support FGF23-mediated catabolism of vitamin D metabolites.
Article in Kidney international, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 40 citations in OpenAlex.
- Differential effects of phosphate binders on vitamin D metabolism in chronic kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2020Trial
- Vitamin D Signaling in Neurodegenerative Disorders: Mechanisms, Therapeutic Potential, and Clinical Implications.Nutrients · 2026Review
- The metabolism of 1,25(OH)Scientific reports · 2022Article
- Non-classical Vitamin D Actions for Renal Protection.Frontiers in medicine · 2021Review
- Ferric citrate reduces fibroblast growth factor 23 levels and improves renal and cardiac function in a mouse model of chronic kidney disease.Kidney international · 2019Article
- Urine albumin and serum uric acid are important determinants of serum 25 hydroxyvitamin D level in pre-dialysis chronic kidney disease patients.Renal failure · 2019Article
- Genetic background influences cardiac phenotype in murine chronic kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2018Article
- Fibroblast Growth Factor 23 Regulation by Systemic and Local Osteoblast-Synthesized 1,25-Dihydroxyvitamin D.Journal of the American Society of Nephrology : JASN · 2017Article
- Gene-by-Diet Interactions Affect Serum 1,25-Dihydroxyvitamin D Levels in Male BXD Recombinant Inbred Mice.Endocrinology · 2016Article
- Efficacy and safety of body weight-adapted oral cholecalciferol substitution in dialysis patients with vitamin D deficiency.BMC nephrology · 2015Article
- Decreased conversion of 25-hydroxyvitamin D3 to 24,25-dihydroxyvitamin D3 following cholecalciferol therapy in patients with CKD.Clinical journal of the American Society of Nephrology : CJASN · 2014Article
- Activation of FGF-23 mediated vitamin D degradative pathways by cholecalciferol.The Journal of clinical endocrinology and metabolism · 2014Article
- Estimated GFR and circulating 24,25-dihydroxyvitamin D3 concentration: a participant-level analysis of 5 cohort studies and clinical trials.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2014Article
- Osteoblast-specific deletion of Pkd2 leads to low-turnover osteopenia and reduced bone marrow adiposity.PloS one · 2014Article
- Calcium regulates FGF-23 expression in bone.Endocrinology · 2013Article
- FGF23 and mineral metabolism in the early post-renal transplantation period.Pediatric nephrology (Berlin, Germany) · 2013Article
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8 authors at 2 institutions in 1 country.
Funding
Abstract
Progressive elevations of fibroblastic growth factor 23 (FGF23) in chronic kidney disease may reduce serum 25-hydroxyvitamin D (25(OH)) and 1,25-dihydroxyvitamin D (1,25(OH)(2)D) levels, via stimulation of 24-hydroxylase (Cyp24a1)-mediated catabolism of these vitamin D metabolites. To test this possibility, we measured serum concentrations of 24,25-dihydroxyvitamin D (24,25(OH)(2)D), a product of Cyp24a1 hydroxylation of 25(OH)D, in the Col4a3 knockout mouse, a model of Alport syndrome-derived chronic kidney disease, and in patients with chronic kidney disease of variable severity. There was an inverse correlation between serum FGF23 and both 25(OH)D and 1,25(OH)(2)D in the mouse model, but no significant relationship was observed in the cross-sectional patient cohort. The FGF23-dependent increase in Cyp24a1 mRNA expression in the mouse kidneys was consistent with the possibility that FGF23 induces vitamin D catabolism. There was, however, a reduction in serum 24,25(OH)(2)D levels, rather than the expected elevation, in both the mice and patients with chronic kidney disease. Low 25(OH)D and elevated FGF23 and parathyroid hormone levels were correlated with the reduced serum 24,25(OH)(2)D concentrations of these patients. Thus, we failed to find support for FGF23-mediated catabolism of vitamin D metabolites in chronic kidney disease assessed by 24,25(OH)(2)D levels.
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