The metabolism of 1,25(OH)2D3 in clinical and experimental kidney disease
Chronic kidney disease (CKD) results in calcitriol deficiency and altered vitamin D metabolism. The objective of this study was to assess the 24-hydroxylation-mediated metabolism of 25(OH)D 3 and 1,25(OH) 2 D 3 in a cross-sectional analysis of participants with a range of kidney function assessed by...
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Veröffentlicht in: | Scientific reports 2022-06, Vol.12 (1), p.10925-10925, Article 10925 |
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Sprache: | eng |
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Zusammenfassung: | Chronic kidney disease (CKD) results in calcitriol deficiency and altered vitamin D metabolism. The objective of this study was to assess the 24-hydroxylation-mediated metabolism of 25(OH)D
3
and 1,25(OH)
2
D
3
in a cross-sectional analysis of participants with a range of kidney function assessed by precise measured GFR (mGFR) (N = 143) and in rats with the induction and progression of experimental kidney disease. Vitamin D metabolites were assessed with LC–MS/MS. Circulating measures of 24-hydroxylation of 25(OH)D
3
(24,25(OH)
2
D
3
:25(OH)D
3
) precisely decreased according to mGFR in humans and progressively in rats with developing CKD. In contrast, the 1,24,25(OH)3D3: 1,25(OH)
2
D
3
vitamin D metabolite ratio increased in humans as the mGFR decreased and in rats with the induction and progression of CKD. Human participants taking cholecalciferol had higher circulating 1,24,25(OH)
3
D
3
, despite no increase of 1,25(OH)
2
D
3
. This first report of circulating 1,24,25(OH)
3
D
3
in the setting of CKD provides novel insight into the uniquely altered vitamin D metabolism in this setting. A better understanding of the uniquely dysfunctional catabolic vitamin D profile in CKD may guide more effective treatment strategies. The potential that 24-hydroxylated products have biological activity of is an important area of future research. |
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ISSN: | 2045-2322 2045-2322 |
DOI: | 10.1038/s41598-022-15033-9 |