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(Hypertension. 2008;52:211.)
© 2008 American Heart Association, Inc.

Editorial Commentaries

Is Activated Vitamin D Supplementation Renoprotective?

From the Division of Nephrology, University of Maryland Medical Systems, Baltimore.

Correspondence to Matthew R. Weir, Division of Nephrology, University of Maryland Medical Systems, 22 S Greene St, Rm N3W143, Baltimore, MD 21201. E-mail mweir@medicine.umaryland.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

If activated vitamin D supplementation is renoprotective, is it because of suppression of the parathyroid hormone (PTH) or selective vitamin D receptor activation?

In the present issue of Hypertension, Alborzi et al¹ present the results of a well-done prospective clinical trial to evaluate the effects of short-term (1-month) treatment with activated vitamin D (paricalcitol) on blood pressure, biomeasures of inflammation, endothelial function, and measures of urinary protein excretion. The results are fascinating. As others have noted previously,² there is an unmistakable effect in reducing urinary protein excretion and also on C-reactive protein levels. Yet, intriguingly, there is no apparent effect on blood pressure, measured either in the office or with 24-hour ambulatory blood pressure monitoring, nor was there an effect on renal hemodynamics, vascular function, or PTH levels.

The combination of persistently high PTH levels and low 1,25-dihydroxyvitamin D levels has been reported to be associated with bone loss, cardiovascular disease, immunosuppression, and increased mortality in patients with end-stage kidney disease.^3,4 Recent studies in patients with chronic kidney disease (CKD) or end-stage kidney disease have suggested that paricalcitol (a selective activator of the vitamin D receptor) is associated with improved mortality.⁵ The explanation for this potential benefit is elusive. Some have suggested that vitamin D receptor activation may mitigate the effects of arterial calcification and possibly even prevent or ameliorate factors leading to atherosclerosis.³ The later benefits may be related to suppression of inflammation, inhibition of bone loss, or possibly attenuation of the activity of the renin-angiotensin system and . . . [Full Text of this Article]