Cardiovascular Effects of Unilateral Nephrectomy in Living Kidney Donors
Identifieur interne : 000094 ( Pmc/Curation ); précédent : 000093; suivant : 000095Cardiovascular Effects of Unilateral Nephrectomy in Living Kidney Donors
Auteurs : William E. Moody ; Charles J. Ferro ; Nicola C. Edwards ; Colin D. Chue ; Erica Lai Sze Lin ; Robin J. Taylor ; Paul Cockwell ; Richard P. Steeds ; Jonathan N. TownendSource :
- Hypertension [ 0194-911X ] ; 2016.
Abstract
Supplemental Digital Content is available in the text.
Url:
DOI: 10.1161/HYPERTENSIONAHA.115.06608
PubMed: 26754643
PubMed Central: 4716285
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PMC:4716285Le document en format XML
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<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Hypertension</journal-id>
<journal-id journal-id-type="iso-abbrev">Hypertension</journal-id>
<journal-id journal-id-type="publisher-id">HYP</journal-id>
<journal-title-group><journal-title>Hypertension</journal-title>
</journal-title-group>
<issn pub-type="ppub">0194-911X</issn>
<issn pub-type="epub">1524-4563</issn>
<publisher><publisher-name>Lippincott, Williams & Wilkins</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">26754643</article-id>
<article-id pub-id-type="pmc">4716285</article-id>
<article-id pub-id-type="art-access-id">00025</article-id>
<article-id pub-id-type="doi">10.1161/HYPERTENSIONAHA.115.06608</article-id>
<article-categories><subj-group subj-group-type="hwp-journal-coll"><subject>10021</subject>
<subject>10041</subject>
<subject>10195</subject>
</subj-group>
<subj-group subj-group-type="heading"><subject>Original Articles</subject>
<subj-group><subject>Kidney</subject>
</subj-group>
</subj-group>
</article-categories>
<title-group><article-title>Cardiovascular Effects of Unilateral Nephrectomy in Living Kidney Donors</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Moody</surname>
<given-names>William E.</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Ferro</surname>
<given-names>Charles J.</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Edwards</surname>
<given-names>Nicola C.</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Chue</surname>
<given-names>Colin D.</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Lin</surname>
<given-names>Erica Lai Sze</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Taylor</surname>
<given-names>Robin J.</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Cockwell</surname>
<given-names>Paul</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Steeds</surname>
<given-names>Richard P.</given-names>
</name>
</contrib>
<contrib contrib-type="author" corresp="yes"><name><surname>Townend</surname>
<given-names>Jonathan N.</given-names>
</name>
</contrib>
<aff>From the Birmingham Cardio-Renal Group, Institute of Cardiovascular Science, Departments of Cardiology (W.E.M., N.C.E., C.D.C., E.L.S.L., R.J.T., R.P.S., J.N.T.) and Nephrology (C.J.F., P.C.), Queen Elizabeth Hospital Birmingham and University of Birmingham, Edgbaston, United Kingdom.</aff>
</contrib-group>
<contrib-group><contrib contrib-type="author"><collab>on behalf of the CRIB-Donor Study Investigators</collab>
</contrib>
</contrib-group>
<author-notes><corresp id="c1">Correspondence to Jonathan N. Townend, Birmingham Cardio-Renal Group, Institute of Cardiovascular Science, Nuffield House, Queen Elizabeth Hospital Birmingham, Edgbaston, B15 2TH, United Kingdom. E-mail <email xlink:href="john.townend@uhb.nhs.uk">john.townend@uhb.nhs.uk</email>
</corresp>
</author-notes>
<pub-date pub-type="ppub"><month>2</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="epub"><day>03</day>
<month>1</month>
<year>2016</year>
</pub-date>
<volume>67</volume>
<issue>2</issue>
<fpage>368</fpage>
<lpage>377</lpage>
<permissions><copyright-statement>© 2016 The Authors.</copyright-statement>
<copyright-year>2016</copyright-year>
<license license-type="open-access"><license-p><italic>Hypertension</italic>
is published on behalf of the American Heart Association, Inc., by Wolters Kluwer. This is an open access article under the terms of the <ext-link ext-link-type="uri" xlink:href="https://creativecommons.org/licenses/by/3.0/">Creative Commons Attribution</ext-link>
License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited.</license-p>
</license>
</permissions>
<self-uri xlink:type="simple" xlink:href="hyp-67-368.pdf"></self-uri>
<abstract abstract-type="toc"><p>Supplemental Digital Content is available in the text.</p>
</abstract>
<abstract><sec><title>Abstract—</title>
<p>There is a robust inverse graded association between glomerular filtration rate (GFR) and cardiovascular risk, but proof of causality is lacking. Emerging data suggest living kidney donation may be associated with increased cardiovascular mortality although the mechanisms are unclear. We hypothesized that the reduction in GFR in living kidney donors is associated with increased left ventricular mass, impaired left ventricular function, and increased aortic stiffness. This was a multicenter, parallel group, blinded end point study of living kidney donors and healthy controls (n=124), conducted from March 2011 to August 2014. The primary outcome was a change in left ventricular mass assessed by magnetic resonance imaging (baseline to 12 months). At 12 months, the decrease in isotopic GFR in donors was −30±12 mL/min/1.73m<sup>2</sup>
. In donors compared with controls, there were significant increases in left ventricular mass (+7±10 versus −3±8 g; <italic>P</italic>
<0.001) and mass:volume ratio (+0.06±0.12 versus −0.01±0.09 g/mL; <italic>P</italic>
<0.01), whereas aortic distensibility (−0.29±1.38 versus +0.28±0.79×10<sup>−3</sup>
mm Hg<sup>−1</sup>
; <italic>P</italic>
=0.03) and global circumferential strain decreased (−1.1±3.8 versus +0.4±2.4%; <italic>P</italic>
=0.04). Donors had greater risks of developing detectable highly sensitive troponin T (odds ratio, 16.2 [95% confidence interval, 2.6–100.1]; <italic>P</italic>
<0.01) and microalbuminuria (odds ratio, 3.8 [95% confidence interval, 1.1–12.8]; <italic>P</italic>
=0.04). Serum uric acid, parathyroid hormone, fibroblast growth factor-23, and high-sensitivity C-reactive protein all increased significantly. There were no changes in ambulatory blood pressure. Change in GFR was independently associated with change in left ventricular mass (<italic>R</italic>
<sup>2</sup>
=0.28; <italic>P</italic>
=0.01). These findings suggest that reduced GFR should be regarded as an independent causative cardiovascular risk factor.</p>
</sec>
<sec><title>Clinical Trial Registration—</title>
<p>URL: <ext-link ext-link-type="uri" xlink:href="http://www.clinicaltrials.gov">http://www.clinicaltrials.gov</ext-link>
. Unique identifier: NCT01028703.</p>
</sec>
</abstract>
<kwd-group><kwd>blood pressure</kwd>
<kwd>glomerular filtration rate</kwd>
<kwd>heart ventricles</kwd>
<kwd>left ventricular remodeling</kwd>
<kwd>vascular stiffness</kwd>
</kwd-group>
<custom-meta-group><custom-meta><meta-name>OPEN-ACCESS</meta-name>
<meta-value>TRUE</meta-value>
</custom-meta>
</custom-meta-group>
</article-meta>
</front>
</pmc>
</record>
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