Several papers indicate that CKD has a problem with poor VDR activation

Vitamin D receptor activation: implications for daily practice.

Contrib Nephrol. 2011;171:172-80. Epub 2011 May 23.
Warnock DG.
Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 34294-0007, USA. dwarnock at uab.edu

Many clinical studies have focused on the relationship between outcome events and serum 25-OH vitamin D levels, despite the fact that most effects are mediated by vitamin D receptor (VDR) activation, the most proximate ligand for which is 1,25-OH(2) vitamin D. Evaluation of the separate components of this axis are well described, but an integrated view of the components, and the distinctions between the effects and consequences of substrate deficiency (25-OH vitamin D), and the direct effects of VDR activation, is the center of focus and ultimately impacts on the clinical approach to patents with chronic kidney disease (CKD). The focus of this contribution is on the specially defined need for vitamin D treatment in patients with CKD, and the importance of VDR activation in CKD, especially in patients with proteinuria. With the addition of the fibroblast growth factor-23 loop, and the realization that albuminuria represents several critical integrated levels of renal function, there is an emerging emphasis on the proximal tubule, interstitial inflammation and fibrosis. These interacting factors reflect fundamental mechanisms that culminate in progressive loss of kidney function(s), with loss of the glomerular filtration rate the most prominent feature. New therapeutic approaches could potentially intervene along these pathways, but they will have to be rigorously evaluated with defined outcome studies and cost-benefit ratio analyses. The ultimate impact of chronic renal replacement therapy and cardiorenal death are the measures by which all such innovations must be judged.
Copyright © 2011 S. Karger AG, Basel.
PMID: 21625108
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Vitamin D receptor activation: clinical outcomes.

Contrib Nephrol. 2011;171:166-71. Epub 2011 May 23.
Covic A, Apetrii M.
Nephrology Clinic, Parhon University Hospital, Gr.T. Popa University of Medicine and Pharmacy, Iasi, Romania. adrianccovic at gmail.com

Vitamin D has been recognized for years as a key player in the control of bone metabolism through the regulation of calcium and phosphate homeostasis. Vitamin D deficiency appears to be common in the general population as a result of decreased dietary intake, diminished absorption, or limited exposure to sunlight. Vitamin D deficiency results in increased circulating levels of parathyroid hormone, which has several disadvantageous effects on bone metabolism. The intake of ordinary doses of vitamin D supplements appears to be associated with a decrease in total mortality rates. In the chronic kidney disease (CKD) population, vitamin D receptor (VDR) activation deficiency is even more severe than in a non-CKD population, with a 25-(OH) vitamin D level being an independent predictor of all-cause mortality. Similarly to nonrenal populations, the corrections of vitamin D deficiency/treatment with vitamin D is associated with better survival.

Selective VDR activators appears to be better than calcitriol in terms of survival or adverse effects.
Copyright © 2011 S. Karger AG, Basel.
PMID: 21625107
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