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Hypertension. 2014 Nov;64(5):1005-11. doi: 10.1161/HYPERTENSIONAHA.114.03748. Epub 2014 Aug 4.

Paricalcitol and endothelial function in chronic kidney disease trial.

Author information

1
From the Nephrology, Hypertension, and Renal Transplantation Unit, Ospedali Riuniti, Reggio Calabria, Italy (C.Z., V.P., F.M.); CNR-IBIM/IFC Clinical Epidemiology and Pathophysiology of Renal Diseases and Hypertension, Reggio Calabria, Italy (C.Z., G.C., V.P., R.T., P.P., M.V., D.B., S.C., R.P., G.T., F.M.); Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy (L.G.); and Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston (R.T.). carmine.zoccali@tin.it.
2
From the Nephrology, Hypertension, and Renal Transplantation Unit, Ospedali Riuniti, Reggio Calabria, Italy (C.Z., V.P., F.M.); CNR-IBIM/IFC Clinical Epidemiology and Pathophysiology of Renal Diseases and Hypertension, Reggio Calabria, Italy (C.Z., G.C., V.P., R.T., P.P., M.V., D.B., S.C., R.P., G.T., F.M.); Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy (L.G.); and Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston (R.T.).

Erratum in

Abstract

Altered vitamin D metabolism and low levels of the active form of this vitamin, 1,25-dihydroxy-vitamin D, is a hallmark of chronic kidney disease (CKD), but there is still no randomized controlled trial testing the effect of active forms of vitamin D on vascular function in patients with CKD. Paricalcitol and ENdothelial fuNction in chronic kidneY disease (PENNY) is a double-blinded randomized controlled trial (ClinicalTrials.gov, NCT01680198) testing the effect of an active form of vitamin D, paricalcitol (2 μg/d×12 weeks) on endothelium-dependent and endothelium-independent vasodilatation in 88 patients with stage 3 to 4 CKD and parathormone >65 pg/mL (paricalcitol, n=44; placebo, n=44). Paricalcitol treatment reduced parathormone (-75 pg/mL; 95% confidence interval, -90 to -60), whereas parathormone showed a small rise during placebo (21 pg/mL; 95% confidence interval, 5-36). Blood pressure did not change in both study arms. Baseline flow-mediated dilation was identical in patients on paricalcitol (3.6±2.9%) and placebo (3.6±2.9%) groups. After 12 weeks of treatment, flow-mediated dilation rose in the paricalcitol but not in the placebo group, and the between-group difference in flow-mediated dilation changes (the primary end point, 1.8%; 95% confidence interval, 0.3-3.1%) was significant (P=0.016), and the mean proportional change in flow-mediated dilation was 61% higher in paricalcitol-treated patients than in placebo-treated patients. Such an effect was abolished 2 weeks after stopping the treatment. No effect of paricalcitol on endothelium-independent vasodilatation was registered. Paricalcitol improves endothelium-dependent vasodilatation in patients with stage 3 to 4 CKD. Findings in this study support the hypothesis that vitamin D may exert favorable effects on the cardiovascular system in patients with CKD.

KEYWORDS:

atherosclerosis; chronic kidney disease; endothelium; hypertension; paricalcitol; vitamin D

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