), West Africans (WA, ), and African Americans (AA, ).
There were significant differences by ancestry: HDLc was positively associated with eGFR in HC (, ), but negatively associated among African ancestry populations (WA: −0.19, ; AA: −0.09, ). These differences were also seen in nationally-representative NHANES data (among European Americans: 0.09, ; among African Americans −0.14, ). To further explore the findings in African ancestry populations, we investigated the role of an African ancestry-specific nephropathy risk variant, rs73885319, in the gene encoding HDL-associated APOL1. Among AA, an inverse HDLc-eGFR association was observed only with the risk genotype (−0.38 versus 0.001; ). This interaction was not seen in WA.
In summary, counter to expectation, an inverse HDLc-eGFR association was observed among those of African ancestry. Given the APOL1 × HDLc interaction among AA, genetic factors may contribute to this paradoxical association. Notably, these findings suggest that the unexplained mechanism by which APOL1 affects kidney-disease risk may involve HDLc.
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<h2 class="articleHeader__specialIssue_title">肾脏疾病在弱势群体中</h2><一个href="//www.newsama.com/journals/ijn/si/159037/" class="articleHeader__specialIssue_url" target="_blank" rel="noreferrer">把这个特殊的问题</一个></d我v>
<strong>临床研究|<gydF4y2Ba!-- -->开放获取</年代trong><d我v class="articleHeader__meta">
<span>体积<gydF4y2Ba!-- -->2012年<gydF4y2Ba!-- -->|</年代pan>
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<h1 class="articleHeader__title">的变化<我>APOL1</gydF4y2Ba我>导致Ancestry-Level HDLc-Kidney功能的差异</h1><d我v class="articleHeader__authors">
<span class="articleHeader__authors_author"><strong>艾米丽贝卡·宾利</年代trong><一个href="//www.newsama.com/cdn-cgi/l/email-protection" aria-label="Mail Option"><span role="img" class="anticon">
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<span class="articleHeader__authors_author">哈尔曼氏崖爬藤p Doumatey<gydF4y2Ba!-- -->,<年代up>1</年代up></span>
<span class="articleHeader__authors_author">Guanjie陈<gydF4y2Ba!-- -->,<年代up>1</年代up></span>
<span class="articleHeader__authors_author">汉虾黄<gydF4y2Ba!-- -->,<年代up>1</年代up></span>
<span class="articleHeader__authors_author">杰周<gydF4y2Ba!-- -->,<年代up>1</年代up></span>
<span class="articleHeader__authors_author">丹尼尔Shriner<gydF4y2Ba!-- -->,<年代up>1</年代up></span>
<span class="articleHeader__authors_author">CongQing江<gydF4y2Ba!-- -->,<年代up>2</年代up></span>
<span class="articleHeader__authors_author">Zhenjian张<gydF4y2Ba!-- -->,<年代up>2</年代up></span>
<span class="articleHeader__authors_author">Guozheng刘<gydF4y2Ba!-- -->,<年代up>2</年代up></span>
<span class="articleHeader__authors_author">Olufemi Fasanmade<gydF4y2Ba!-- -->,<年代up>3</年代up></span>
<span class="articleHeader__authors_author">托马斯•约翰逊<gydF4y2Ba!-- -->,<年代up>3</年代up></span>
<span class="articleHeader__authors_author">和<gydF4y2Ba!-- -->约翰尼奥利<年代up>4</年代up><i>et al。</我></年代pan>
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<strong>学术编辑器:</年代trong><年代pan>鲁道夫·a·罗德里格斯</年代pan>
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<strong>收到了</年代trong><年代pan>07年2月2012年</年代pan>
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<strong>修改后的</年代trong><年代pan>2012年6月26日</年代pan>
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<div class="articleHeader__timeline_item ">
<strong>接受</年代trong><年代pan>2012年7月11日</年代pan>
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<strong>发表</年代trong><年代pan>2012年9月02</年代pan>
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<h4 class="header" id="abstract">文摘</h4><gydF4y2Bap>低水平的高密度胆固醇(为)伴随慢性肾脏疾病,但是为之间的关系和估计的肾小球滤过率(eGFR)在普通人群中尚不清楚。我们调查了非糖尿病的汉族人的HDLc-eGFR协会(HC,<年代vg height="10.9125" id="M1" style="vertical-align:-0.17555pt;width:58.537498px;" version="1.1" viewbox="0 0 58.537498 10.9125" width="58.537498" xmlns="http://www.w3.org/2000/svg">
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=</t年代pan>
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1</t年代pan>
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</svg>;非洲裔美国人−0.14,<年代vg height="10.9125" id="M9" style="vertical-align:-0.17555pt;width:56.150002px;" version="1.1" viewbox="0 0 56.150002 10.9125" width="56.150002" xmlns="http://www.w3.org/2000/svg">
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</svg>)。这种交互是佤邦未见。总之,与期望,逆HDLc-eGFR协会观察那些非洲血统。考虑到<我>APOL1</gydF4y2Ba我>×为交互中AA,遗传因素可能导致这种似是而非的协会。值得注意的是,这些发现表明,原因不明的机制<我>APOL1</gydF4y2Ba我>影响肾脏疾病风险可能包括为。</gydF4y2Bap>
<span class="end-abs"></span>
<h4 id="introduction">1。介绍</h4><gydF4y2Bap>血脂异常是一种已知的相关的慢性肾脏疾病(CKD),增加甘油三酯(TG)、高密度脂蛋白胆固醇下降(为)持续观察<一个href="#B1">1</一个>,<gydF4y2Ba一个href="#B2">2</一个>]。脂质与肾功能之间的关系一般人群中,然而,不太清楚。血脂异常的反应肾小球和血管细胞之间是相似的(<一个href="#B3">3</一个>),一个atherosclerosis-like机制损害已经提出了肾功能不全(<一个href="#B2">2</一个>,<gydF4y2Ba一个href="#B4">4</一个>和一直支持的动物模型<一个href="#B5">5</一个>]。血脂异常可能导致肾功能的恶化。当然预防CKD激励进一步说明这种关系,肾功能监测疾病风险的意义超出。常见的肾功能指标,估计肾小球滤过率(eGFR)与心血管疾病和全因死亡率(<一个href="#B6">6</一个>- - - - - -<一个href="#B9">9</一个>)甚至有轻度到中度的肾功能亏损(<一个href="#B6">6</一个>,<gydF4y2Ba一个href="#B7">7</一个>]。</gydF4y2Bap>
<p>有一致的报道成反比TG (<一个href="#B10">10</一个>- - - - - -<一个href="#B14">14</一个>在较小程度上),总胆固醇(<一个href="#B14">14</一个>,<gydF4y2Ba一个href="#B15">15</一个>与肾脏功能)。然而,为协会尚不明朗。积极为和肾功能之间的联系已经观察到(<一个href="#B10">10</一个>,<gydF4y2Ba一个href="#B12">12</一个>,<gydF4y2Ba一个href="#B14">14</一个>- - - - - -<一个href="#B16">16</一个>)符合atherosclerosis-like模型;然而,最近的报道发现逆为和肾功能之间的联系(<一个href="#B11">11</一个>,<gydF4y2Ba一个href="#B17">17</一个>)尽管这种关系是未知的生物机制。</gydF4y2Bap>
<p>项目中使用的各种方法,这种关系提供证据,很难确定这些变化协会是真实的群体差异的结果,特定的肾功能措施考虑,或者分析策略。因此,我们评估了为与肾功能之间的关系在不同人群有目的地设计一致的数据和生物样本采集和分析相同。</gydF4y2Bap>
<p></p>
<p>考虑不同人群尤其在描述HDLc-kidney函数相关协会有几个原因。首先,CKD的利率(及其发展为终末期肾病(ESRD)人口和血统有很大不同,原因尚不清楚。例如,在美国,非洲裔美国人有慢性肾病的风险高出近三倍<一个href="#B18">18</一个>),非洲和亚洲美国人ESRD的比率高于欧洲的美国人(高3.7倍和1.3倍,分别地)(<一个href="#B19">19</一个>]。非裔美国人有一个大约5倍的速度从肾功能不全进展的迹象比欧洲的美国人(<一个href="#B20">20.</一个>]。另一个动机为研究这种关系在不同人群的血脂水平的变化在不同的遗传背景。尤其是非洲血统的人群,大大降低为,TC, TG分布比欧洲血统同行。这些差异的原因尚不清楚,但可能意味着不同的脂质和疾病之间的关系。这种差异的存在是“under-identification”支持的非洲人和非裔美国人的代谢综合征的脂质标准:高血压、2型糖尿病和心血管疾病的风险仍然很高在这些人群的“正常”的TG值(<一个href="#B21">21</一个>,<gydF4y2Ba一个href="#B22">22</一个>]。</gydF4y2Bap>
<p>最近发现的错义变异<我>载脂蛋白L1</我>基因(<我>APOL1</gydF4y2Ba我>),增加肾脏疾病的风险<一个href="#B23">23</一个>非洲裔美国人)使HDLc-kidney函数协会的理解非常及时。变异的基因编码这HDLc-associated脂蛋白存在相对较高的频率在非洲血统的人群,和被认为是增加分布由于保护优势对非洲昏睡病的严重。这种变异影响肾脏疾病风险的机制,根据最近的一份报告中,同种异体移植肾移植后生存(<一个href="#B24">24</一个>),尚未阐明。我们调查血清为之间的关系和西非人表皮生长因子受体在三个独立的流行病学研究中,非裔美国人,汉族。非洲人,非洲裔美国人和西部nephropathy-associated的角色<我>APOL1</gydF4y2Ba我>r年代73885319变体,也是评估。</gydF4y2Bap>
<h4 id="methods">2。方法</h4><h5gydF4y2Baid="sec2.1">2.1。研究参与者</h5><gydF4y2Bap>伦理批准为每一个研究从负责任的机构审查委员会(IRB)获得在每个研究站点/机构,霍华德大学,美国国立卫生研究院。所有科目为样本的收集提供了书面知情同意和随后的分析。本研究是根据表达的原则进行的《赫尔辛基宣言》。</gydF4y2Bap>
<p>参与者来自三个独立的流行病学研究:非洲美国糖尿病(AADM)研究中,霍华德大学家庭研究(霍夫),美国和中国糖尿病研究(CADM)。进一步的细节AADM [<一个href="#B25">25</一个>和霍夫<一个href="#B26">26</一个>)曾被发表。简而言之,AADM是一个大规模的病例对照研究,旨在探索2型糖尿病的遗传和环境因素(T2D)在西非。霍夫以人群为基础的研究无关的家庭和非裔美国人登记从华盛顿特区大都市。CADM大规模遗传流行病学研究旨在探讨T2D的遗传和环境因素无关的中国汉族人从随州地区。参与者完成了问卷中所使用的相同的AADM和霍夫(用适当的文化适应性),参加诊所访问。T2D情况下,定义为在physician-prescribed糖尿病治疗或与空腹血糖≥126 mg / dl在不止一个场合,被排除在目前的调查。</gydF4y2Bap>
<p>有4574 non-T2D跨三个研究参与者。其中381名参与者被丢失或极端的血清脂质测量。额外的排除了协变量缺失<年代vg height="14.225" id="M11" style="vertical-align:-2.7337pt;width:365.97501px;" version="1.1" viewbox="0 0 365.97501 14.225" width="365.97501" xmlns="http://www.w3.org/2000/svg">
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</svg>。排除后,4136名参与者被认为是主要的分析。主要研究结果也在全国代表性调查全国健康和营养调查(NHANES)多年来,2007 - 2008,和2003 - 2004<一个href="#B27">27</一个>,<gydF4y2Ba一个href="#B28">28</一个>)(2005- 2006年数据不包括被观察到的不良倾向为试验(<一个href="#B29">29日</一个>])。排除后,623年非洲裔美国人(NHAA)和1709年欧洲美国人(NHEA)包括(参与者两年调查分析)。</gydF4y2Bap>
<h5 id="sec2.2">2.2。实验室</h5><gydF4y2Bap>血清脂质(TG、TC和为)测定酶使用方法标准化的内部和其他适当的参考方法(例如,疾病预防控制中心为参考方法,同位素稀释质谱法(ID-MS) TC和TG)。为是化验使用均相酶比色测定所有军团(COBAS Integra 400罗氏诊断,在美国(WA, AA);AEROSET C8000、雅培诊断、中国(HC)和罗氏/日立模块化P化学分析仪,罗氏诊断,在美国(NHANES)。年龄组计算(使用Friedewald方程)(<一个href="#B30">30.</一个>]。</gydF4y2Bap>
<p>佤邦,AA, NHANES,血清肌酐水平测定使用Jaffe反应没有除蛋白要么COBAS Integra 400分析仪(美国在罗氏诊断;佤邦和AA)或贝克曼同步分析仪(美国贝克曼库尔特公司CA;NHANES)。在HC,血清肌酐是化验AEROSET C8000(雅培诊断,中国)使用一个酶促反应。制造商进行的方法比较表明,两种方法产生可接受的相关性(<年代vg height="11.0375" id="M12" style="vertical-align:-0.27588pt;width:53.237499px;" version="1.1" viewbox="0 0 53.237499 11.0375" width="53.237499" xmlns="http://www.w3.org/2000/svg">
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</g>
</svg>:参考,<一个href="http://www.accessdata.fda.gov/cdrh_docs/pdf7/K073634.pdf" target="_blank">http://www.accessdata.fda.gov/cdrh_docs/pdf7/K073634.pdf</一个>)。这些方法已经标准化对ID /女士和主要参考资料(SRM 914)。</gydF4y2Bap>
<h5 id="sec2.3">2.3。基因分型</h5><gydF4y2Bap>进一步评估结果,我们组主要的肾脏疾病<我>载脂蛋白L1</我>(<gydF4y2Ba我>APOL1</gydF4y2Ba我>)风险变异(rs73885319) 1296年,非裔美国人(霍夫)和1095西非人(AADM)。基因分型结果进行MassArray平台上使用iPLEX黄金分析(Sequenom,圣地亚哥,CA)如前所述[<一个href="#B31">31日</一个>]。简而言之,PCR引物设计和扩展使用MassArray设计软件,序列信息是从公共数据库编目snp进口。该平台使用化学碱基引物延伸与MALDI-TOF女士的检测技术。这个SNP的平均通话率在AADM霍夫的98.1%和97.2%。在成功输入个人,基因型频率在HWE<年代vg height="13.6375" id="M13" style="vertical-align:-2.21957pt;width:66.550003px;" version="1.1" viewbox="0 0 66.550003 13.6375" width="66.550003" xmlns="http://www.w3.org/2000/svg">
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<tspan style="font-size: 12.50px; " x="0" y="0">
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0</t年代pan>
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。</t年代pan>
<tspan style="font-size: 12.50px; " x="36.471252" y="0">
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<tspan style="font-size: 12.50px; " x="48.974251" y="0">
)</t年代pan>
</text>
</g>
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</svg>和一致性复制基因型> 99.9%。</gydF4y2Bap>
<h5 id="sec2.4">2.4。统计分析</h5><gydF4y2Bap>我们作为衡量肾功能估计的肾小球滤过率(eGFR),这是计算根据种族和性别慢性肾病协作方程(<一个href="#B32">32</一个>]。不是正态分布的变量转换(BMI和脂质变量)。饮酒是一分为二的自我报告和一些不经常食用。吸烟代表明确(吸烟,烟民,不抽烟的人)。</gydF4y2Bap>
<p>鉴于血清脂质措施之间的多重共线性和这些和BMI之间,这些变量是mean-centered和规范化。没有观察到多重共线性在转换后的变量。表皮生长因子受体和预测之间的关系进行了分析使用population-stratified线性回归模型调整年龄,年龄<年代up>2</年代up>、性别、体重指数、吸烟、年龄组和TG(包括隔离为协会,而不是相关的血清脂质成分),和酒精使用。对于那些研究与相关参与者(霍夫和AADM),家庭的随机效应调整包括在内。正式评估的差异之间的关系为人口和表皮生长因子受体,所有研究都包括在相同的模型与一个为×研究交互项。</gydF4y2Bap>
<p>发表的研究结果一致(<一个href="#B33">33</一个>),<gydF4y2Ba我>APOL1</gydF4y2Ba我>r年代73885319编码的隐性(在GG,称为“肾病风险基因型”与GA / AA)。关联的基因型为和表皮生长因子受体在线性混合模型确定调整的年龄,年龄<年代up>2</年代up>,并与随机聚类性,家庭。非裔美国人,主成分分析来评估人口结构进行了使用EIGENSOFT [<一个href="#B34">34</一个>),第一主成分代表非洲血统的比例,是保留(如前面报道(<一个href="#B35">35</一个>),包括在rs73885319的所有模型。评估之间的交互<我>APOL1</gydF4y2Ba我>变体,为rs73885319 x为产品添加。所有进行了分析使用SAS 9.2 (SAS研究所,卡里,NC)。数据图形化表示使用R (<一个href="http://www.r-project.org/" target="_blank">http://www.r-project.org/</一个>)。</gydF4y2Bap>
<h4 id="results">3所示。结果</h4><gydF4y2Bap>共有4316名参与者符合入选标准(表<一个href="//www.newsama.com/journals/ijn/2012/748984/tab1/" target="_blank">1</一个>):1497 AADM参与者(西非人:WA);1539霍夫参与者(非洲裔美国人:AA);1100年CADM参与者(汉族:HC)。佤邦最高表皮生长因子受体(<我>P</gydF4y2Ba我><0。0001和HC;<年代vg height="11.0375" id="M14" style="vertical-align:-0.17555pt;width:71.775002px;" version="1.1" viewbox="0 0 71.775002 11.0375" width="71.775002" xmlns="http://www.w3.org/2000/svg">
<g transform="matrix(1.25,0,0,-1.25,0,11.0375)">
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6</t年代pan>
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</svg>对AA)。种群之间的显著差异,血清脂质被观察到。总胆固醇是在佤邦远低于AA或HC<年代vg height="13.45" id="M15" style="vertical-align:-2.21957pt;width:82.1875px;" version="1.1" viewbox="0 0 82.1875 13.45" width="82.1875" xmlns="http://www.w3.org/2000/svg">
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<</t年代pan>
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0</t年代pan>
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。</t年代pan>
<tspan style="font-size: 12.50px; " x="36.471252" y="0">
0</t年代pan>
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0</t年代pan>
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0</t年代pan>
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</svg>,反映出较低意味着为<年代vg height="13.45" id="M16" style="vertical-align:-2.21957pt;width:82.1875px;" version="1.1" viewbox="0 0 82.1875 13.45" width="82.1875" xmlns="http://www.w3.org/2000/svg">
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<g transform="translate(72,-61.24)">
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<tspan style="font-size: 12.50px; " x="0" y="0">
(</t年代pan>
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<tspan style="font-size: 12.50px; " x="15.053612" y="0">
<</t年代pan>
<tspan style="font-size: 12.50px; " x="27.094002" y="0">
0</t年代pan>
<tspan style="font-size: 12.50px; " x="33.345501" y="0">
。</t年代pan>
<tspan style="font-size: 12.50px; " x="36.471252" y="0">
0</t年代pan>
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0</t年代pan>
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0</t年代pan>
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1</t年代pan>
<tspan style="font-size: 12.50px; " x="61.477249" y="0">
)</t年代pan>
</text>
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</svg>。甘油三酯是高度可变的三项研究中,佤邦有15 mg / dl平均浓度低于AA和近50 mg / dl平均浓度低于HC (<我>P</gydF4y2Ba我>所有比较p < 0.0001)。降低意味着TG水平一直在非洲——比欧洲或亚洲血统人口(<一个href="#B36">36</一个>- - - - - -<一个href="#B42">42</一个>]。</gydF4y2Bap>
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<span class="caption-text">表1</年代pan>
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参与者特征的群体<年代up>1</年代up>。</d我v>
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<p>为和表皮生长因子受体之间的不同研究之间的关系(图<一个href="//www.newsama.com/journals/ijn/2012/748984/fig1/" target="_blank">1</一个>)。最值得注意的是,虽然为与表皮生长因子受体在每一个研究中,有关协会的方向不同,在佤邦与逆协会(<我><我>β</gydF4y2Ba我></我>−0.19,<gydF4y2Ba我>P</gydF4y2Ba我><0。0001),AA (<我><我>β</gydF4y2Ba我></我>−0.09,<gydF4y2Ba我>P</gydF4y2Ba我>在HC = 0.02)和积极的协会(<我><我>β</gydF4y2Ba我></我>0.13,<gydF4y2Ba我>P</gydF4y2Ba我><0。0001)。</gydF4y2Bap>
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<td>高阶资料连结控制和表皮生长因子受体在不同人群之间的联系。为协会和西非人表皮生长因子受体(WA),非裔美国人(从霍华德大学家庭研究中,AA),非裔美国人(来自全国健康和营养调查,NHAA),汉族(HC),欧洲的美国人(NHEA)。线性模型调整年龄,年龄<年代up>2</年代up>、性别、体重指数、甘油三酯、年龄组、饮酒和吸烟(家庭佤邦和AA)和随机效应。</td></tr></tbody>
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<p>正如所料,当所有研究都包括在一个模型中,一个为×研究相互作用非常显著<年代vg height="13.45" id="M17" style="vertical-align:-2.21957pt;width:82.1875px;" version="1.1" viewbox="0 0 82.1875 13.45" width="82.1875" xmlns="http://www.w3.org/2000/svg">
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<g transform="translate(72,-61.24)">
<text transform="matrix(1,0,0,-1,-71.95,63.5)">
<tspan style="font-size: 12.50px; " x="0" y="0">
(</t年代pan>
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<tspan style="font-size: 12.50px; " x="15.053612" y="0">
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0</t年代pan>
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1</t年代pan>
<tspan style="font-size: 12.50px; " x="61.477249" y="0">
)</t年代pan>
</text>
</g>
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</svg>。依然如此当只有两项研究被认为是一次(佤邦与AA (<我>P</gydF4y2Ba我>=0。001),佤邦与HC (<我>P</gydF4y2Ba我><0。0001),AA和HC (<我>P</gydF4y2Ba我><0。0001))。</gydF4y2Bap>
<p>确定为研究结果的普遍性,分析运行在欧洲的美国人,非洲裔美国人从NHANES (NHEA NHAA, resp)。这些发现支持结果发现在最初的分析:为与表皮生长因子受体在NHEA呈正相关(<我>β</gydF4y2Ba我>:0.09,<我>P</gydF4y2Ba我>=0。005)和消极NHAA中表皮生长因子受体(<我>β</gydF4y2Ba我>:−0.14,P = 0.03)。</gydF4y2Bap>
<p>进一步评估意想不到,但一致,不同协会的非洲血统,rs73885319之间的关系,一个SNP,非洲裔美国人与肾脏疾病有关,研究了AA和佤邦。nephropathy-associated等位基因的频率(GG) 0.21和0.38在AA和佤邦,分别。</gydF4y2Bap>
<p>没有证据表明变量之间的关联和表皮生长因子受体在人口(图<一个href="//www.newsama.com/journals/ijn/2012/748984/fig2/" target="_blank">2</一个>)。虽然没有观察协会之间的变异,为人口作为一个整体,在女性中,有一些证据HDLc AA女性不同的基因型(5.3 mg / dl更高风险基因型),尽管这仍没有统计上显著的调整后为多个测试<年代vg height="16.987499" id="M18" style="vertical-align:-5.04861pt;width:103.55px;" version="1.1" viewbox="0 0 103.55 16.987499" width="103.55" xmlns="http://www.w3.org/2000/svg">
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d</t年代pan>
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j</t年代pan>
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u</t年代pan>
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年代</t年代pan>
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t</t年代pan>
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</svg>。一个正式的测试性别×rs73885319交互作用不显著<年代vg height="13.45" id="M19" style="vertical-align:-2.21957pt;width:66.550003px;" version="1.1" viewbox="0 0 66.550003 13.45" width="66.550003" xmlns="http://www.w3.org/2000/svg">
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<td>意思是为非洲裔美国人,rs73885319表皮生长因子受体基因型和西部AfricansMean为,rs73885319表皮生长因子受体基因型(GG =肾病风险基因型),从线性混合效应模型估计调整年龄、年龄<年代up>2</年代up>、性别、和整体的比例掺合料(非洲裔美国人),与随机聚类家庭。没有统计上显著差异HDLc或表皮生长因子受体基因型。</td></tr></tbody>
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<p>AA参与者,统计上显著的变体之间的交互和观察为:逆为与表皮生长因子受体与风险较大的那些基因型相比,那些没有(<我>β</gydF4y2Ba我>:−0.38和0.001,<年代vg height="14.7125" id="M20" style="vertical-align:-3.22281pt;width:103.5375px;" version="1.1" viewbox="0 0 103.5375 14.7125" width="103.5375" xmlns="http://www.w3.org/2000/svg">
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</svg>;图<一个href="//www.newsama.com/journals/ijn/2012/748984/fig3/" target="_blank">3</一个>)。结果不变的BMI,年龄组,TG到模型中。这种交互在佤邦没有被观察到<年代vg height="14.7125" id="M21" style="vertical-align:-3.22281pt;width:106.1375px;" version="1.1" viewbox="0 0 106.1375 14.7125" width="106.1375" xmlns="http://www.w3.org/2000/svg">
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<td>之间的联系为非洲裔美国人表皮生长因子受体和西非人rs73885319基因型<gydF4y2Bab>。</gydF4y2Bab>修改为和表皮生长因子受体之间的联系的rs73885319基因型(GG =肾病风险基因型),估计的线性混合模型为×rs73885319,调整为rs73885319,年龄、年龄<年代up>2</年代up>、性别、和整体的比例掺合料(非洲裔美国人),与随机聚类家庭。那些肾病的风险基因型,协会更消极的比那些没有这种基因型(<我>β</gydF4y2Ba我>:−0.38和0.001,<年代vg height="14.7125" id="M22" style="vertical-align:-3.22281pt" version="1.1" viewbox="0 0 103.5375 14.7125" width="103.5375" xmlns="http://www.w3.org/2000/svg">
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<h5 id="sec3.1">3.1。敏感性分析</h5><gydF4y2Bap>解决潜在的担心患病的参与者把观察到的结果(不排除是为当前慢性肾病)进行敏感性分析排除那些eGFR < 60毫升/分钟/ 1.73米<年代up>2</年代up>:方向和HDL-eGFR协会的统计显著性改变。同样,有证据表明,方程用于估计肾小球滤过率(GFR) (<一个href="#B32">32</一个>]只有两个层面为亚洲或非洲黑人种族并不准确(<一个href="#B43">43</一个>]。当我们用一个方程,包括一个独特的亚洲系数(<一个href="#B43">43</一个>]HC和消除了“黑色”系数WA(系数发现产生更多的偏见比省略在南非黑人(<一个href="#B43">43</一个>]),HDL-eGFR结果不变。同样,当使用可观察到没有区别MDRD方程估计肾小球滤过率(GFR)而不是CKD-EPI方程(<一个href="#B44">44</一个>]。降脂药物可能影响肾小球滤过率(GFR)和高密度脂蛋白浓度。虽然这些药物的使用是几乎不存在的西非人(AADM)和未知的中国(CADM) ~ 4%的非洲裔美国人(霍夫)参与者使用这些药物。当分析仅限于与降脂药物的使用数据子集的非洲裔美国人(78%的参与者),这一项纳入模型没有影响的大小,方向,或感兴趣的关联的统计学意义。</gydF4y2Bap>
<p>虽然HDL-eGFR NHANES AA的结果,不包括亲戚、符合观察是什么在佤邦和霍夫AA,其中也包括亲戚,我们进行了灵敏度分析调查的可能性亲缘的调整我们的模型是不足以消除一个潜在的偏见。当只有无关的参与者包括高密度脂蛋白之间的关系和表皮生长因子受体是类似的,仍然显著。在霍夫rs73885319交互的分析仅限于无关的参与者,效果是类似的,虽然<我>P-</我>价值增加<年代vg height="13.45" id="M23" style="vertical-align:-2.21957pt;width:58.737499px;" version="1.1" viewbox="0 0 58.737499 13.45" width="58.737499" xmlns="http://www.w3.org/2000/svg">
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</svg>。一致的效应大小和减少统计学意义表明,这种差异是由于样本容量的减少,而不是偏见,类似的结论进一步支持的结果在前面的运行分析随机相关数据集的子集。因此,没有证据,推断出基于包含相关的个人偏见的两个样品评估。</gydF4y2Bap>
<p>此外,没有发现变化观察到的结果与调整高血压,高血压治疗,或c反应蛋白(CRP在AADM或CADM)。直言血清脂类变量的使用并没有提供额外的洞察力,尽管这些观察结果一致与连续变量的分析。不一致的模式的观察分析地层内重复时血清脂质进一步描述的关系。</gydF4y2Bap>
<p>解决潜在的担心ethnicity-specific eGFR估计方程的偏差可能导致一个明显不同的协会的祖先,我们再做分析使用血清肌酐作为结果。结果与报道的观察一致(逆HDLc-eGFR协会在非洲以外的祖先群体和积极的协会非洲血统组)。</gydF4y2Bap>
<h4 id="discussion">4所示。讨论</h4><gydF4y2Bap>在这个西非(WA)的调查,非裔美国人(AA),和汉族(HC)成年人,肾功能之间的关系,为通过祖先显著不同:HC中观察到积极的协会,和两个非洲血统人群存在负相关。一个已知nephropathy-associated变体(rs73885319)<我>APOL1</gydF4y2Ba我>基因编码一个HDL-associated载脂蛋白,AA之间的研究。在AA女性中,高为观察那些nephropathy-associated基因型。进一步说,在非洲裔美国男性和女性中,逆为和表皮生长因子受体之间的联系只是观察到的基因型风险。</gydF4y2Bap>
<p>的不一致的方向HDLc-eGFR协会在佤邦和AA HC相比当前冲突的文献是一个重要的贡献。这个变化,一直收集和相同的数据分析中发现三个独立的流行病学研究表明,人口水平变化的关系。支持这些发现,积极的协会被发现在一个代表性的欧裔美国人(NHEA),而逆协会在一个类似的代表性的非裔美国人(NHAA)。同意我们的发现在非洲以外的祖先种群,低高密度脂蛋白与慢性肾病的发病率增加有关日本(<一个href="#B14">14</一个>与肌酐升高)和跟踪主要是欧洲的美国人(<一个href="#B15">15</一个>]。相比之下,在荷兰成年人,为和载脂蛋白a - 1与肾功能呈负相关<一个href="#B17">17</一个>]。在非洲人的唯一之前研究[<一个href="#B11">11</一个>),结果支持我们的发现在非洲血统人群:为是肾功能在南非黑人成负相关。两个民族的研究评估HDLc-kidney函数,观察到一个积极的关系<一个href="#B10">10</一个>,<gydF4y2Ba一个href="#B12">12</一个>)(只在未经调整模型(<一个href="#B12">12</一个>])。然而,这些研究报告评估的种族/民族互动或分层分析。事实上,一些研究包括多个种族只是调整”比赛,“没有报告正式评估不同协会的种族(即。通过测试一个交互项)。演示执行这些详细的分析的重要性,我们评估了HC和AA在一起,用一个调整民族(种族和为没有交互项):没有为协会和表皮生长因子受体<年代vg height="13.45" id="M24" style="vertical-align:-2.21957pt;width:58.737499px;" version="1.1" viewbox="0 0 58.737499 13.45" width="58.737499" xmlns="http://www.w3.org/2000/svg">
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</svg>。同样的,当所有三个种群被认为在一起,有一个逆HDLc-eGFR协会<年代vg height="13.45" id="M25" style="vertical-align:-2.21957pt;width:82.1875px;" version="1.1" viewbox="0 0 82.1875 13.45" width="82.1875" xmlns="http://www.w3.org/2000/svg">
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</svg>,尽管强大,仅在HC观察到显著正相关。没有评价的交互项,这些数据会让我们得出这样的结论:没有为协会和表皮生长因子受体(HC和AA)或协会可以被描述为一个强大的、逆为与表皮生长因子受体(HC、AA和佤邦),结论不合适给我们分析。</gydF4y2Bap>
<p>同时积极为协会和表皮生长因子受体在非洲以外的祖先群体是一致的期望更高的为与各种良好的健康状况有关,逆协会观察到佤邦和两个AA人群是出乎意料的时候。一种可能是由基因决定的高密度脂蛋白粒子的特征或其相关的蛋白质不同的非洲和非洲以外的祖先的方式不会被检测到的比较为浓度。例如,变化可能存在抗氧化或消炎作用的高密度脂蛋白或粒子的大小分布的方式相关的肾脏功能。据报道,非洲血统的通常有一个更有利的脂质粒子的大小分布比非非洲血统的<一个href="#B45">45</一个>- - - - - -<一个href="#B47">47</一个>]。虽然还不清楚HDL颗粒大小如何影响肾功能,这些已知的差异在一个高密度脂蛋白粒子的非洲血统的特征值得考虑我们的发现。不幸的是,我们没有可用的数据来测试这些假设。</gydF4y2Bap>
<p>另一个可能性是与肾脏功能为只有一种间接关系,而是其他由基因决定性状的生物标志物更向近端与肾脏功能有关,而这特征(或这个特质之间的关系,为)显著不同的祖先。进一步支持这一假设来自最近的发现为心肌梗死(MI)的风险,相关疾病模型考虑到肾小球和血管细胞已被证明同样应对血脂异常(<一个href="#B3">3</一个>]。虽然保护为和心脏病之间的联系是众所周知,基因变异,提高为没有MI的风险减少大约21000例病例和95000例对照(<一个href="#B48">48</一个>),强调了这种完善的关联的潜在的生物机制需要进一步调查。值得注意的是,非洲裔美国人通常更健康的血脂不转化为心血管疾病的患病率较低,冠心病和中风的非洲裔美国人相差只有~ 1%相比,欧洲的美国人(<一个href="#B49">49</一个>]。它也是有用的考虑血清脂质和胰岛素抵抗(IR)的关系。血清脂类,尤其是TG和为,与红外光谱在欧洲血统的人,但越来越多的证据支持非洲血统的不同或缺席协会个人(综述[<一个href="#B50">50</一个>- - - - - -<一个href="#B53">53</一个>])。连同这些发现,我们的研究结果建议需要增加注意为在疾病中的作用,主要侧重于不同的种族。</gydF4y2Bap>
<p><i>APOL1</我>变异,包括rs73885319,被认为已在非洲血统人群中高频区域的锥虫病流行,因为这些变异赋予保护一种致命的非洲昏睡病(这些变体几乎缺席non-African-ancestry人群)。尽管有保护作用<我>APOL1</gydF4y2Ba我>变异在传染病的背景下,这些变异是有害的慢性疾病背景:通过未知的机制,变异增加肾病的风险在非洲裔美国人<一个href="#B33">33</一个>]。在这个分析中,我们表明,nephropathy-associated变体修改为和表皮生长因子受体之间的关系在非洲裔美国人,这样一个逆协会只是观察到那些风险基因型。很难推测关于观察交互背后的生物机制考虑到已知的强劲这种变体和肾病协会非裔美国人尚未解开。变异的HDL-associated蛋白质如何授予保护非洲昏睡病影响肾脏疾病是未知的,但是他们的发现表明高密度脂蛋白和肾脏之间的联系,没有很好地开发。值得注意的是,最近的一项研究报告的非裔美国人的浓度下降中高密度脂蛋白粒子之间的那些<我>APOL1</gydF4y2Ba我>风险变异<一个href="#B54">54</一个>]。在我们的研究中,总共没有区别为或表皮生长因子受体基因型检测。如果变异形式的<我>APOL1</gydF4y2Ba我>影响小分支分布,这种变更或另一个variant-provoked扰乱肾功能变化,这些发现可能对我们的研究结果提供了一个解释。其他可能的解释包括eGFR变异的产生影响,导致下游变化HDLc或者变体分别影响这两个量。解开了观察到的关联的潜在的生物机制超出了本研究设计的范围,但是在这个领域中做进一步的工作是迫切需要洞察这种关系可能产生重大影响的筛查和治疗肾脏疾病在非洲裔美国人。</gydF4y2Bap>
<p>西非人缺乏互动的原因(尽管他们的基因相似),尚不清楚,尽管这些种群之间有许多差异,可以进一步探讨。表皮生长因子受体的分布,为不同AA与佤邦相比,即使调整(图反是<一个href="//www.newsama.com/journals/ijn/2012/748984/fig2/" target="_blank">2</一个>),建议的可能性,只是在特定水平的明显的交互为或表皮生长因子受体。此外,有广泛的参数差异AA和佤邦(例如,饮食、传染病曝光,吸烟,和肥胖),其中之一将提供必要的生物环境,产生观察效果。</gydF4y2Bap>
<p>感兴趣的,有证据表明性别的影响分析。具体地说,在非洲裔美国人、欧洲人,汉族,关系更紧密的观察在妇女和HDLc-eGFR协会的差异<我>APOL1</gydF4y2Ba我>基因型在女性非裔美国人也更强。虽然大多数以前的研究不报告HDL-kidney函数中性别差异的评价,更强大的协会在最近的两项研究观察女性,观察逆为协会和肾脏功能<一个href="#B11">11</一个>,<gydF4y2Ba一个href="#B17">17</一个>]。一些相关建议的途径进一步考虑性别差异。estrogen-signaled更改的结果,更大的脂肪储存,并增加游离脂肪酸动员、有一个双重的大VLDL进入女性的循环,增加VLDL传输和删除导致类似的意思是VLDL但更高的浓度为<一个href="#B55">55</一个>]。这种增强新陈代谢可能导致更大的对扰动的敏感性。同时,除了拥有一个高的平均浓度为的比例为存在高密度脂蛋白颗粒较高的女性一样大(<一个href="#B46">46</一个>]。虽然,目前尚不清楚如何粒度分布的差异可能会影响肾脏功能,值得注意的是这个假设也遵循新发现的微分分布的高密度脂蛋白子类<我>APOL1</gydF4y2Ba我>基因型(<一个href="#B54">54</一个>]。</gydF4y2Bap>
<p>群体差异受到广泛的潜在的混杂因素,使索赔血统的差异难以自信地断言。虽然有显著差异群体中考虑环境因素和生活方式因素,进一步考虑收益率支持祖先的差异。首先,所有模型都是调整的吸烟、饮酒,和身体质量指数;三个因素,重要的是组间和不同可能影响HDL和表皮生长因子受体(尽管从问卷数据充分代表生活方式特征的局限性是承认)。此外,潜在的混杂的生活方式和文化因素是不相似的非裔美国和西非人口HDLc-eGFR协会是一致的。而吸烟,例如,非洲裔美国人非常高,几乎没有出现在西部非洲。肥胖率是同样的,完全不同的西非洲人和非裔美国人之间,并存病、饮酒、降脂药物的使用(西非人之间几乎不存在的)。很难想象生活方式因素将更多的非洲裔美国人高度相关和西非人比欧洲和非洲裔美国人之间的美国人,和协会可以解释观察到的模式。考虑到类似的祖先但不同环境因素的非裔美国人和西方非洲人,一直观察到逆为和表皮生长因子受体之间的联系支持推理共享遗传因素的作用。</gydF4y2Bap>
<p>我们的调查有一些显著的优点:(1)三项研究都是由相同的研究人员所作的设计,问卷的使用故意设计成类似,尽可能考虑到不同文化背景的问题;(2)有一个非洲裔美国人的人口以及西非祖先的人口提供了一个绝佳的机会来研究复杂疾病风险的上下文中类似的祖先背景和高度不同的生活方式和文化风险。本研究的一些局限性,可能会或可能不会直接影响的解释观察到的结果是值得讨论:(1)我们没有调整教育和收入等社会经济因素的价值观和社会语境中的值的影响将比较研究(教育水平,例如,有显著不同的影响参与者的医疗使用、饮食和生活方式因素这三个研究的网站);(2)横断面的分析让人无法确定观察到的关联结果从肾小球滤过率(GFR)下降的作用为浓度或成长为对表皮生长因子受体的影响;(3)HDL不是为特征的炎性或氧化剂能力或粒子大小、特征可能是关键在理解观察到的关系。然而,在研究人群生活方式的分布特点,将影响HDL的氧化剂或炎症状态不符合这些作为一个解释观察到的结果:氧化剂因素(吸烟和肥胖)的比率高城市非裔美国样本,吸烟也是相当高的汉族(在观察人积极的协会),和吸烟比率非常低和BMI分布更为温和的西非人(谁最强的逆协会观察)。最后,在非洲裔美国人的另一个示例是复制必要的确认观察rs73885319和为之间的互动。</gydF4y2Bap>
<p>总之,这个分析报告协会不同人群的血清脂质和肾功能。为和表皮生长因子受体之间的关联的方向不同的血统,与一个积极的协会在汉族和欧洲的美国人,和逆协会西部非洲人和非裔美国人。虽然这些群体差异背后的因素是未知的,nephropathy-associated变体<我>APOL1</gydF4y2Ba我>修改HDLc-eGFR协会在非洲裔美国人强烈逆协会中观察到的基因型风险,而没有协会观察无风险的基因型。进一步研究调查的作用<我>APOL1</gydF4y2Ba我>变异在肾脏疾病应该探索的影响<我>APOL1</gydF4y2Ba我>高阶资料连结控制。</gydF4y2Bap>
<h4 id="acknowledgments">确认</h4><gydF4y2Bap>本文的内容是完全的责任作者,不一定代表美国国立卫生研究院的官方观点。支持的研究拨款s06gm008016 - 320107 c . Rotimi和s06gm008016 - 380111 a . Adebowale,来自美国/ mbr /评分程序。参与者人数进行了霍华德大学一般临床研究中心,这是由格兰特2号m01rr010284从国家研究资源中心,美国国立卫生研究院的一个组成部分。这项研究支持部分由校内研究项目,国家人类基因组研究所的研究中心的基因组学和全球卫生(CRGGH-Z01HG200362)。CRGGH还支持由国家糖尿病、消化和肾脏疾病研究所(NIDDK),信息技术中心,美国国立卫生研究院办公室主任。支持非洲美国糖尿病(AADM)研究是国家少数民族研究所提供的健康和健康差异,趋势和NHGRI。投资者没有参与研究设计、数据收集和分析,决定发表,或准备的手稿。</gydF4y2Bap>
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