In chronic kidney disease (CKD), the loss of renal capacity to maintain the integrity of the vitamin D endocrine system accelerates skeletal, immune, renal, and cardiovascular aging to increase mortality rates. This chapter updates the CKD-induced abnormalities in vitamin D bio-activation to 1,25(OH)2D, which compromise 1,25(OH)2D pro-survival actions and increase the risk of vitamin D toxicity. Focus is given to advances in CKD-driven impairment of 1,25(OH)2D-vitamin D receptor (VDR) complex pro-survival actions including (1) Suppression of parathyroid hormone (PTH) gene expression, parathyroid gland hyperplasia, and PTH-driven cardiovascular damage; (2) Attenuation of bone loss; (3) Induction of the fibroblast growth factor 23 (FGF23)/klotho axis; and (4) Attenuation of hypertension and systemic inflammation. This knowledge is essential to resolve controversies in evaluating vitamin D status during CKD and to identify biomarkers of 1,25(OH)2D/VDR action distinct from PTH to design personalized vitamin D interventions that safely and effectively delay CKD onset and/or attenuate its progression and complications.

Original languageEnglish
Title of host publicationFeldman and Pike's Vitamin D
Subtitle of host publicationVolume Two: Disease and Therapeutics
Number of pages32
ISBN (Electronic)9780323913386
ISBN (Print)9780323913393
StatePublished - Jan 1 2023


  • 1,25(OH)D
  • ACE2
  • ADAM17
  • Cardiovascular disease
  • Chronic kidney disease
  • FGF23
  • Hypertension
  • Klotho
  • Parathyroid hormone
  • Systemic inflammation
  • Vitamin D receptor


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