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The assumption has been that 1,25(OH)2D is solely responsible for calcium absorption. That has been one of the presumed causes of hyperparathyroidism in chronic kidney disease (CKD) (low 1,25(OH)2D leads to decreased calcium absorption, which increases parathyroid hormone release in compensation). Replacing 1,25 D directly has been the goal with using 1,25D or its analogues in CKD. There is very little data concerning use of native vitamin D or 25(OH)D in CKD, although autocrine functions in extrarenal tissues would use 25(OH)D. The latest KDIGO guidelines do recognize the autocrine role of vitamin D, but have no data on outcomes or doses or optimal levels to guide them and so have made a blanket recommendation to treat 25D levels in CKD by general healthy population guidelines.
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