Background: Vitamin D deficiency is highly prevalent and associated with secondary hyperparathyroidism in patients with chronic kidney disease (CKD). The Kidney Disease Outcomes Quality Initiative (K/DOQI) guidelines recommend treatment of vitamin D deficiency starting with CKD stage 3, though no data are available showing an impact on serum parathyroid hormone (PTH) concentrations. The goal of this analysis, therefore, was to determine the effect of ergocalciferol treatment on plasma PTH concentrations in vitamin D-deficient patients with stage 3 and stage 4 CKD. Methods: A prospective, nonrandomized observational analysis was conducted in an academic community hospital CKD clinic. Fifty-two patients with stage 3 or stage 4 CKD with vitamin D deficiency and elevated PTH concentrations received ergocalciferol dosed per a modified K/DOQI guidelines protocol and adjusted every 3 months. Serum PTH, 25-vitamin D, 1,25-vitamin D, calcium, phosphorus, and albumin levels were drawn at initiation of therapy and repeated every 3 months. Results: The mean 25-vitamin D levels normalized in patients with stage 3 and 4 CKD, with values of 31.6 ± 2.2 ng/ml (78.8 ± 5.49 nmol/l) and 35.4 ± 1.9 ng/ml (88.4 ± 4.74 nmol/l), respectively (p < 0.0001). A median decrease in PTH concentrations of 13.1 and 2.0% was noted in patients with stage 3 and stage 4 CKD, respectively (p = 0.041, p = nonsignificant). Conclusions: Ergocalciferol therapy is a reasonable initial therapy for vitamin D deficiency associated with elevated PTH levels in stage 3 CKD. It does not appear to have equivalent benefits in stage 4 CKD.

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We describe a case of rapid onset of vascular calcification coincident with the initiation of warfarin therapy in a kidney transplant patient. Calcification developed within the media of the blood vessel wall, with relative intimal sparing. Medium and small sized arteries were affected, but the aorta was mostly free of calcifications, suggesting a differential response to warfarin between the intima and media as well as between different vascular beds. In addition, unlike the highly calcified native kidney's vessels, the kidney allograft was not calcified, suggesting local, genetically determined, mechanisms in preventing vascular calcification. Distal subcutaneous necrosis ultimately lead to the patient's demise. Index wordsvascular calcification; warfarin; hemodialysis; MGP Vascular calcification is a major contributor to the morbidity and mortality of end-stage renal disease (ESRD) patients. Whereas atherosclerosis typically involves the vessel intima, ESRD patients are particularly susceptible to a form of vascular calcification involving the media and elastic lamina of large and medium sized arteries. Recently, vitamin K dependent proteins have gained recognition as important components in this process. 1 MGP (matrix Gla protein) acts as a potent vascular calcification inhibitor, and Gas6 (growth arrestspecific 6) controls vascular smooth muscle cell death and calcification. Both are produced by vascular smooth muscle cells, and undergo post-translational carboxylation in order to become biologically active, a process requiring sufficient levels of reduced vitamin K, as well as several important enzymes, including vitamin K epoxide reductase and gammaglutamylcarboxylase. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.Financial Disclosure: The authors declare that they have no relevant financial interests. NIH Public Access Author ManuscriptAm J Kidney Dis. Author manuscript; available in PMC 2011 December 1. Warfarin, widely used as an anticoagulant, interferes with the post-translational modification of vitamin K dependent proteins, rendering them inactive. Although its anticoagulant effect has gained widespread therapeutic use, less is known about its potential side effect on vitamin K dependent proteins within the vasculature. In animal models, warfarin administration, albeit at supraphysiological doses, induces widespread medial vascular calcification 2 . Its clinical use has been associated with the development of calciphylaxis 3 , a form of metastatic small vessel calcification, aortic valve and coronary calcification 4 , and stroke 5 .We describe a cas...

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