GW24-e3533 Correlation between C171T mutation of KCNJ5 gene and hypokalemic in patients with primary aldosteronism

Objectives To investigate the correlation between C171T mutation of the potassium inwardly-rectifying channel, subfamily J, member 5 (KCNJ5) gene, and the hypokalemic primary aldosteronism (PA). Methods A total of 364 patients with PA were classified into hypokalemic group (n = 115) and normokalemic...

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Veröffentlicht in:Heart (British Cardiac Society) 2013-08, Vol.99 (Suppl 3), p.A11-A11
Hauptverfasser: Hongjian, Li, Delian, Zhang, Feiya, Zu, Guijuan, Chang, Jianqiong, Kong, Keming, Zhou, Junli, Hu, Qin, Luo, Nuerguli, Xiangyang, Zhang, Nan-fang, Li
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container_end_page A11
container_issue Suppl 3
container_start_page A11
container_title Heart (British Cardiac Society)
container_volume 99
creator Hongjian, Li
Delian, Zhang
Feiya, Zu
Guijuan, Chang
Jianqiong, Kong
Keming, Zhou
Junli, Hu
Qin, Luo
Nuerguli
Xiangyang, Zhang
Nan-fang, Li
description Objectives To investigate the correlation between C171T mutation of the potassium inwardly-rectifying channel, subfamily J, member 5 (KCNJ5) gene, and the hypokalemic primary aldosteronism (PA). Methods A total of 364 patients with PA were classified into hypokalemic group (n = 115) and normokalemic group (n = 249). The C171T mutation of KCNJ5 gene in all subjects was genotyped by TaqMan polymerase chain reaction (TaqMan PCR). The correlation between C171T mutation of KCNJ5 gene and hypokalemic PA was analysed. Results The C171T mutation was genotyped successfully in all subjects and was in Hardy-Weinberg equilibrium (P > 0.05). The hypokalemic and normokalemic PA groups showed statistically significant differences in the distributions of genotypes, alleles, and dominant model models of C171T mutation in overall and female patients (P < 0.05). Logistic regression analysis showed that, after adjusting for age, smoking, alcohol consumption and BMI, the CT + TT genotype of C171T mutation was identified as a risk factor of PA by dominant modelling (OR = 2.50, 95% CI: 1.17-5.35, P = 0.018). In female PA patients, the serum potassium level was significantly reduced, while serum aldosterone concentration was significantly increased in (CT + TT) genotype group compared with those in CC genotype group (all P
doi_str_mv 10.1136/heartjnl-2013-304613.25
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Methods A total of 364 patients with PA were classified into hypokalemic group (n = 115) and normokalemic group (n = 249). The C171T mutation of KCNJ5 gene in all subjects was genotyped by TaqMan polymerase chain reaction (TaqMan PCR). The correlation between C171T mutation of KCNJ5 gene and hypokalemic PA was analysed. Results The C171T mutation was genotyped successfully in all subjects and was in Hardy-Weinberg equilibrium (P &gt; 0.05). The hypokalemic and normokalemic PA groups showed statistically significant differences in the distributions of genotypes, alleles, and dominant model models of C171T mutation in overall and female patients (P &lt; 0.05). Logistic regression analysis showed that, after adjusting for age, smoking, alcohol consumption and BMI, the CT + TT genotype of C171T mutation was identified as a risk factor of PA by dominant modelling (OR = 2.50, 95% CI: 1.17-5.35, P = 0.018). In female PA patients, the serum potassium level was significantly reduced, while serum aldosterone concentration was significantly increased in (CT + TT) genotype group compared with those in CC genotype group (all P &lt;0.05). Conclusions The C171T mutation of KCNJ5 gene is associated with the female hypokalemia PA.</description><identifier>ISSN: 1355-6037</identifier><identifier>EISSN: 1468-201X</identifier><identifier>DOI: 10.1136/heartjnl-2013-304613.25</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and British Cardiovascular Society</publisher><ispartof>Heart (British Cardiac Society), 2013-08, Vol.99 (Suppl 3), p.A11-A11</ispartof><rights>2013, Published by the bMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</rights><rights>Copyright: 2013 (c) 2013, Published by the bMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttp://heart.bmj.com/content/99/Suppl_3/A11.1.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttp://heart.bmj.com/content/99/Suppl_3/A11.1.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,314,780,784,3196,23571,27924,27925,77600,77631</link.rule.ids></links><search><creatorcontrib>Hongjian, Li</creatorcontrib><creatorcontrib>Delian, Zhang</creatorcontrib><creatorcontrib>Feiya, Zu</creatorcontrib><creatorcontrib>Guijuan, Chang</creatorcontrib><creatorcontrib>Jianqiong, Kong</creatorcontrib><creatorcontrib>Keming, Zhou</creatorcontrib><creatorcontrib>Junli, Hu</creatorcontrib><creatorcontrib>Qin, Luo</creatorcontrib><creatorcontrib>Nuerguli</creatorcontrib><creatorcontrib>Xiangyang, Zhang</creatorcontrib><creatorcontrib>Nan-fang, Li</creatorcontrib><title>GW24-e3533 Correlation between C171T mutation of KCNJ5 gene and hypokalemic in patients with primary aldosteronism</title><title>Heart (British Cardiac Society)</title><addtitle>Heart</addtitle><description>Objectives To investigate the correlation between C171T mutation of the potassium inwardly-rectifying channel, subfamily J, member 5 (KCNJ5) gene, and the hypokalemic primary aldosteronism (PA). Methods A total of 364 patients with PA were classified into hypokalemic group (n = 115) and normokalemic group (n = 249). The C171T mutation of KCNJ5 gene in all subjects was genotyped by TaqMan polymerase chain reaction (TaqMan PCR). The correlation between C171T mutation of KCNJ5 gene and hypokalemic PA was analysed. Results The C171T mutation was genotyped successfully in all subjects and was in Hardy-Weinberg equilibrium (P &gt; 0.05). The hypokalemic and normokalemic PA groups showed statistically significant differences in the distributions of genotypes, alleles, and dominant model models of C171T mutation in overall and female patients (P &lt; 0.05). Logistic regression analysis showed that, after adjusting for age, smoking, alcohol consumption and BMI, the CT + TT genotype of C171T mutation was identified as a risk factor of PA by dominant modelling (OR = 2.50, 95% CI: 1.17-5.35, P = 0.018). In female PA patients, the serum potassium level was significantly reduced, while serum aldosterone concentration was significantly increased in (CT + TT) genotype group compared with those in CC genotype group (all P &lt;0.05). Conclusions The C171T mutation of KCNJ5 gene is associated with the female hypokalemia PA.</description><issn>1355-6037</issn><issn>1468-201X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkMlOwzAURSMEEuM3YIl1wENsJ0tIoQwFNmUQG8tJX2naxC62K2DHhh_lS0gUYM3qDTr3DTeK9gk-JISJoxloF-amjikmLGY4EYQdUr4WbZFEpF33cb3NGeexwExuRtvezzHGSZaKrSgMH2gSA-OMfX185tY5qHWorEEFhFcAg3IiyRg1q9C37RRd5TeXHD2DAaTNBM3el3aha2iqElUGLVsOTPDotQoztHRVo9070vXE-gDOmso3u9HGVNce9n7iTnR3djrOz-PR7fAiPx7FBeFSxFlCMhB0SjNCISmBQykmqSwwFmVaZkVJBSGaScpLTXGLas61KAhOddaVbCc66OcunX1ZgQ9qblfOtCsVkSmWjHLeUbKnSme9dzBVP0crglVnsfq1WHUWq95iRXmrjHtl1b729ifTbqGEZJKrm_tcjZ-uR8OrwYkatDzt-aKZ_3vJN3l-kMg</recordid><startdate>201308</startdate><enddate>201308</enddate><creator>Hongjian, Li</creator><creator>Delian, Zhang</creator><creator>Feiya, Zu</creator><creator>Guijuan, Chang</creator><creator>Jianqiong, Kong</creator><creator>Keming, Zhou</creator><creator>Junli, Hu</creator><creator>Qin, Luo</creator><creator>Nuerguli</creator><creator>Xiangyang, Zhang</creator><creator>Nan-fang, Li</creator><general>BMJ Publishing Group Ltd and British Cardiovascular Society</general><general>BMJ Publishing Group LTD</general><scope>BSCLL</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope></search><sort><creationdate>201308</creationdate><title>GW24-e3533 Correlation between C171T mutation of KCNJ5 gene and hypokalemic in patients with primary aldosteronism</title><author>Hongjian, Li ; Delian, Zhang ; Feiya, Zu ; Guijuan, Chang ; Jianqiong, Kong ; Keming, Zhou ; Junli, Hu ; Qin, Luo ; Nuerguli ; Xiangyang, Zhang ; Nan-fang, Li</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b1576-9419e62f2912e4ce5ec6d87b006c8c9bc2611a3725ca209e6a55a6b108a909e63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hongjian, Li</creatorcontrib><creatorcontrib>Delian, Zhang</creatorcontrib><creatorcontrib>Feiya, Zu</creatorcontrib><creatorcontrib>Guijuan, Chang</creatorcontrib><creatorcontrib>Jianqiong, Kong</creatorcontrib><creatorcontrib>Keming, Zhou</creatorcontrib><creatorcontrib>Junli, Hu</creatorcontrib><creatorcontrib>Qin, Luo</creatorcontrib><creatorcontrib>Nuerguli</creatorcontrib><creatorcontrib>Xiangyang, Zhang</creatorcontrib><creatorcontrib>Nan-fang, Li</creatorcontrib><collection>Istex</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><jtitle>Heart (British Cardiac Society)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hongjian, Li</au><au>Delian, Zhang</au><au>Feiya, Zu</au><au>Guijuan, Chang</au><au>Jianqiong, Kong</au><au>Keming, Zhou</au><au>Junli, Hu</au><au>Qin, Luo</au><au>Nuerguli</au><au>Xiangyang, Zhang</au><au>Nan-fang, Li</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>GW24-e3533 Correlation between C171T mutation of KCNJ5 gene and hypokalemic in patients with primary aldosteronism</atitle><jtitle>Heart (British Cardiac Society)</jtitle><addtitle>Heart</addtitle><date>2013-08</date><risdate>2013</risdate><volume>99</volume><issue>Suppl 3</issue><spage>A11</spage><epage>A11</epage><pages>A11-A11</pages><issn>1355-6037</issn><eissn>1468-201X</eissn><abstract>Objectives To investigate the correlation between C171T mutation of the potassium inwardly-rectifying channel, subfamily J, member 5 (KCNJ5) gene, and the hypokalemic primary aldosteronism (PA). Methods A total of 364 patients with PA were classified into hypokalemic group (n = 115) and normokalemic group (n = 249). The C171T mutation of KCNJ5 gene in all subjects was genotyped by TaqMan polymerase chain reaction (TaqMan PCR). The correlation between C171T mutation of KCNJ5 gene and hypokalemic PA was analysed. Results The C171T mutation was genotyped successfully in all subjects and was in Hardy-Weinberg equilibrium (P &gt; 0.05). The hypokalemic and normokalemic PA groups showed statistically significant differences in the distributions of genotypes, alleles, and dominant model models of C171T mutation in overall and female patients (P &lt; 0.05). Logistic regression analysis showed that, after adjusting for age, smoking, alcohol consumption and BMI, the CT + TT genotype of C171T mutation was identified as a risk factor of PA by dominant modelling (OR = 2.50, 95% CI: 1.17-5.35, P = 0.018). In female PA patients, the serum potassium level was significantly reduced, while serum aldosterone concentration was significantly increased in (CT + TT) genotype group compared with those in CC genotype group (all P &lt;0.05). Conclusions The C171T mutation of KCNJ5 gene is associated with the female hypokalemia PA.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and British Cardiovascular Society</pub><doi>10.1136/heartjnl-2013-304613.25</doi></addata></record>
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title GW24-e3533 Correlation between C171T mutation of KCNJ5 gene and hypokalemic in patients with primary aldosteronism
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