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Effect of paricalcitol on left ventricular mass and function in CKD--the OPERA trial.

Identifieur interne : 000209 ( PubMed/Corpus ); précédent : 000208; suivant : 000210

Effect of paricalcitol on left ventricular mass and function in CKD--the OPERA trial.

Auteurs : Angela Yee-Moon Wang ; Fang Fang ; John Chan ; Yue-Yi Wen ; Shang Qing ; Iris Hiu-Shuen Chan ; Gladys Lo ; Kar-Neng Lai ; Wai-Kei Lo ; Christopher Wai-Kei Lam ; Cheuk-Man Yu

Source :

RBID : pubmed:24052631

English descriptors

Abstract

Vitamin D seems to protect against cardiovascular disease, but the reported effects of vitamin D on patient outcomes in CKD are controversial. We conducted a prospective, double blind, randomized, placebo-controlled trial to determine whether oral activated vitamin D reduces left ventricular (LV) mass in patients with stages 3-5 CKD with LV hypertrophy. Subjects with echocardiographic criteria of LV hypertrophy were randomly assigned to receive either oral paricalcitol (1 μg) one time daily (n=30) or matching placebo (n=30) for 52 weeks. The primary end point was change in LV mass index over 52 weeks, which was measured by cardiac magnetic resonance imaging. Secondary end points included changes in LV volume, echocardiographic measures of systolic and diastolic function, biochemical parameters of mineral bone disease, and measures of renal function. Change in LV mass index did not differ significantly between groups (median [interquartile range], -2.59 [-6.13 to 0.32] g/m(2) with paricalcitol versus -4.85 [-9.89 to 1.10] g/m(2) with placebo). Changes in LV volume, ejection fraction, tissue Doppler-derived measures of early diastolic and systolic mitral annular velocities, and ratio of early mitral inflow velocity to early diastolic mitral annular velocity did not differ between the groups. However, paricalcitol treatment significantly reduced intact parathyroid hormone (P<0.001) and alkaline phosphatase (P=0.001) levels as well as the number of cardiovascular-related hospitalizations compared with placebo. In conclusion, 52 weeks of treatment with oral paricalcitol (1 μg one time daily) significantly improved secondary hyperparathyroidism but did not alter measures of LV structure and function in patients with severe CKD.

DOI: 10.1681/ASN.2013010103
PubMed: 24052631

Links to Exploration step

pubmed:24052631

Le document en format XML

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<div type="abstract" xml:lang="en">Vitamin D seems to protect against cardiovascular disease, but the reported effects of vitamin D on patient outcomes in CKD are controversial. We conducted a prospective, double blind, randomized, placebo-controlled trial to determine whether oral activated vitamin D reduces left ventricular (LV) mass in patients with stages 3-5 CKD with LV hypertrophy. Subjects with echocardiographic criteria of LV hypertrophy were randomly assigned to receive either oral paricalcitol (1 μg) one time daily (n=30) or matching placebo (n=30) for 52 weeks. The primary end point was change in LV mass index over 52 weeks, which was measured by cardiac magnetic resonance imaging. Secondary end points included changes in LV volume, echocardiographic measures of systolic and diastolic function, biochemical parameters of mineral bone disease, and measures of renal function. Change in LV mass index did not differ significantly between groups (median [interquartile range], -2.59 [-6.13 to 0.32] g/m(2) with paricalcitol versus -4.85 [-9.89 to 1.10] g/m(2) with placebo). Changes in LV volume, ejection fraction, tissue Doppler-derived measures of early diastolic and systolic mitral annular velocities, and ratio of early mitral inflow velocity to early diastolic mitral annular velocity did not differ between the groups. However, paricalcitol treatment significantly reduced intact parathyroid hormone (P<0.001) and alkaline phosphatase (P=0.001) levels as well as the number of cardiovascular-related hospitalizations compared with placebo. In conclusion, 52 weeks of treatment with oral paricalcitol (1 μg one time daily) significantly improved secondary hyperparathyroidism but did not alter measures of LV structure and function in patients with severe CKD.</div>
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<CommentsCorrections RefType="Cites">
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<CommentsCorrections RefType="Cites">
<RefSource>J Cardiovasc Magn Reson. 2005;7(5):775-82</RefSource>
<PMID Version="1">16353438</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites">
<RefSource>J Am Soc Echocardiogr. 2005 Dec;18(12):1440-63</RefSource>
<PMID Version="1">16376782</PMID>
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<CommentsCorrections RefType="Cites">
<RefSource>Circulation. 2006 Mar 14;113(10):e396-8</RefSource>
<PMID Version="1">16534017</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites">
<RefSource>BMC Nephrol. 2006;7:2</RefSource>
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<CommentsCorrections RefType="Cites">
<RefSource>J Am Soc Nephrol. 2007 Jan;18(1):321-30</RefSource>
<PMID Version="1">17167121</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites">
<RefSource>N Engl J Med. 2007 Jul 19;357(3):266-81</RefSource>
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<CommentsCorrections RefType="Cites">
<RefSource>Arch Intern Med. 2007 Sep 10;167(16):1730-7</RefSource>
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<CommentsCorrections RefType="Cites">
<RefSource>Ann Intern Med. 2007 Dec 18;147(12):840-53</RefSource>
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