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对高血脂症的认识和看法作文英文回答：High blood lipid disorder, also known as hyperlipidemia or high cholesterol, is a medical condition characterized by elevated levels of lipids (fats) in the blood. It is a common condition that affects millions of people worldwide and is a major risk factor for cardiovascular diseases such as heart attacks and strokes.There are two types of lipids that are commonly measured in a lipid profile: low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol, and high-density lipoprotein (HDL) cholesterol, also known as "good" cholesterol. High levels of LDL cholesterol can lead to the formation of plaque in the arteries, which can restrict blood flow and increase the risk of heart disease. On the other hand, high levels of HDL cholesterol are beneficial as they help remove LDL cholesterol from the bloodstream.Personally, I believe that it is important to have a good understanding of high blood lipid disorder in order to take appropriate measures to prevent and manage it. One of the main causes of high blood lipid disorder is an unhealthy lifestyle, which includes a diet high in saturated and trans fats, lack of physical activity, smoking, and excessive alcohol consumption. By making lifestyle changes such as adopting a healthy diet, engaging in regular exercise, quitting smoking, and moderating alcohol intake, individuals can effectively lower their blood lipid levels and reduce their risk of developing cardiovascular diseases.In addition to lifestyle changes, medication may also be prescribed to manage high blood lipid disorder. Statins are commonly prescribed to reduce LDL cholesterol levels, while fibrates and niacin can help increase HDL cholesterol levels. It is important to note that medication should always be taken under the guidance of a healthcare professional and should be complemented with lifestyle modifications for optimal results.To illustrate the importance of understanding and managing high blood lipid disorder, let me share a personal anecdote. A close family member of mine was diagnosed with high blood lipid disorder a few years ago. Initially, they were not aware of the seriousness of the condition and did not take any measures to manage it. However, after experiencing a heart attack, they realized the importance of making lifestyle changes and taking medication as prescribed. They started following a heart-healthy diet, exercising regularly, and taking medication as directed. As a result, their blood lipid levels improved, and they have not experienced any further cardiovascular events.In conclusion, high blood lipid disorder is a common medical condition that can have serious consequences ifleft unmanaged. It is important to have a good understanding of the condition and take appropriate measures to prevent and manage it. By making lifestyle changes, taking prescribed medication, and regularly monitoring blood lipid levels, individuals can effectively lower their risk of developing cardiovascular diseases associated with high blood lipid disorder.中文回答：高血脂症，又称为高脂血症或高胆固醇，是一种血液中脂质（脂肪）水平升高的医学状况。
非hdc胆固醇标准英文回答：Non-HDL cholesterol is a measure of the cholesterol in your blood that is not carried by high-density lipoprotein (HDL) cholesterol. HDL cholesterol is the "good"cholesterol that helps to remove cholesterol from your arteries and transport it back to your liver. Non-HDL cholesterol, on the other hand, is the "bad" cholesterolthat can build up in your arteries and cause them to narrow.The non-HDL cholesterol goal for adults is less than130 mg/dL. However, your doctor may recommend a lower goalif you have other risk factors for heart disease, such as high blood pressure, diabetes, or a family history of heart disease.There are a number of things you can do to lower your non-HDL cholesterol levels, including:Eating a healthy diet that is low in saturated and trans fats and high in fiber.Getting regular exercise.Losing weight if you are overweight or obese.Quitting smoking.Taking medication to lower your cholesterol, if necessary.中文回答：非高密度脂蛋白胆固醇，是指血液中未被高密度脂蛋白（HDL）胆固醇携带的胆固醇。
高密度脂蛋白胆固醇的相对分子质量高密度脂蛋白胆固醇（High-density lipoprotein cholesterol，HDL-C）是指在血浆中携带胆固醇的一种脂蛋白。
相对分子质量是指一个分子的相对质量与其质子质量之比，用来反映分子的质量大小。
在高密度脂蛋白胆固醇中，相对分子质量的计算主要取决于胆固醇和蛋白质的相对分子质量。
高密度脂蛋白胆固醇是一种非常重要的生物标志物，它在人体内发挥着重要的生理功能。
与低密度脂蛋白胆固醇（LDL-C）相比，高密度脂蛋白胆固醇被认为是一种“好胆固醇”，具有保护心血管健康的作用。
高密度脂蛋白胆固醇通过与其他脂蛋白的相互作用，参与胆固醇的运输和代谢。
高密度脂蛋白胆固醇的相对分子质量主要由两部分组成：胆固醇和蛋白质。
胆固醇是一种脂质，具有多环结构，其相对分子质量约为386.65 g/mol。
胆固醇主要存在于细胞膜中，是细胞膜的重要组成部分，同时也是多种生物活性物质的合成原料。
在高密度脂蛋白胆固醇中，胆固醇通过与蛋白质的结合形成复合物，从而参与胆固醇的运输和代谢。
蛋白质是高密度脂蛋白胆固醇的另一个重要组成部分，具有多样性和复杂性。
蛋白质是生物体内最基本的结构和功能单位，其相对分子质量根据不同的蛋白质而有所不同。
在高密度脂蛋白胆固醇中，蛋白质起到支架和稳定胆固醇的作用，同时也与其他脂蛋白相互作用，参与胆固醇的运输和代谢过程。
高密度脂蛋白胆固醇的相对分子质量对于评估心血管健康非常重要。
研究表明，高密度脂蛋白胆固醇水平与冠心病的发病风险呈负相关。
高密度脂蛋白胆固醇可以通过多种途径保护心血管健康，如促进胆固醇从外周组织向肝脏的反转运输、抗氧化、抗炎和抗凝血等作用。
因此，人们通常将高密度脂蛋白胆固醇作为预防和治疗心血管疾病的重要指标之一。
为了维持高密度脂蛋白胆固醇的相对分子质量在适宜的范围内，人们可以通过合理的饮食和生活方式来调节。
合理的饮食包括减少饱和脂肪酸和胆固醇的摄入，增加富含高密度脂蛋白胆固醇的食物，如鱼类、坚果和橄榄油等。
nafld病理诊断标准全文共四篇示例，供读者参考第一篇示例：非酒精性脂肪肝病（Non-alcoholic fatty liver disease，NAFLD）是一种常见的慢性肝脏疾病，其发病率正逐年增加。
NAFLD包括非酒精性脂肪肝（Non-alcoholic fatty liver，NAFL）和非酒精性脂肪性肝炎（Non-alcoholic steatohepatitis，NASH），后者进展至肝硬化和肝癌的风险更高。
为了更好地诊断和治疗NAFLD，科研人员和临床医生们正不断完善相关的病理诊断标准。
NAFLD的病理诊断主要依靠组织学检查，目前被广泛认可和应用的标准是美国肝病研究协会（AASLD）和欧洲肝脏病学会（EASL）共同发布的指南。
根据这些指南，NAFLD的诊断需要满足以下几个关键标准：1. 脂肪沉积：组织学检查发现肝脏脂质沉积是诊断NAFLD的基本标志。
通常情况下，肝细胞内脂质的沉积程度要大于5%。
病理检查一般采用肝组织活检的方式获取样本，然后通过HE染色或Oil Red O 染色来观察细胞内脂质的沉积情况。
2. 弥漫小胞变性：NAFLD患者的肝细胞脂质沉积常导致细胞内小胞变性，即肝细胞胞浆内含有细小而均匀的脂滴。
这是NAFLD病理学诊断的另一个关键特征。
3. 肝细胞损伤：在NAFLD进展至NASH的过程中，肝细胞常伴有炎症和坏死。
病理学检查会观察肝细胞的炎症细胞浸润、纤维化和坏死等情况，以判断病情的严重程度。
4. 肝纤维化：肝纤维化是NAFLD进展至肝硬化和肝癌的一个主要预警信号。
病理学检查可通过观察肝组织的纤维化程度来评估疾病的进展情况，进而指导治疗方案的选择。
除了以上述关键标准外，病理学家在进行NAFLD病理诊断时还需排除其他引起脂肪肝的原因，如酒精性肝病、病毒性肝炎等。
结合患者的临床病史、实验室检查和影像学检查结果，有助于提高诊断的准确性和综合性。
近年来，一些新的病理诊断技术也逐渐应用于NAFLD的诊断中，如肝脏组织三维重建、传统染色法与免疫组化染色相结合等。
高密度脂蛋白（HDL）拮抗内毒素的实验研究王宁;魏利召【期刊名称】《中国药理通讯》【年(卷),期】2005(022)003【摘要】目的：通过对高密度脂蛋白（HDL）体内外生物学活性实验研究，探讨HDL对内毒素的中和作用。
方法：应用勤和生物传感器技术检测HDL与LPS的结合活性，采用ELISA方法检测HDL对LPS攻击小鼠的保护作用等试验来阐明HDL对LPS的中和效果。
结果：应用亲和生物传感器亲和力检测，结果发现HDL 与lipidA之间具有很高的．木和能力；HDL可以显著抑制LPS刺激小鼠RAW264．7细胞释放TNF—α，并成量效关系；在小鼠体内使用剂量为120mg ／kg的HDL可以明显保护致死剂量LPS攻击小鼠，保护率达到70％。
结论：HDL在体内外与LPS结合，从而抑制了LPS的生物学活性，被认为是一种内毒素清除剂，对防治脓毒症具有临床指导意义，【总页数】2页(P51-52)【作者】王宁;魏利召【作者单位】重庆第三军医大学附属西南医院中心实验室,重庆400038【正文语种】中文【中图分类】R446.112【相关文献】1.地骨皮提取物CL-5拮抗内毒素的实验研究 [J], 伏建峰;曹红卫;龙宇鹏;王宁;刘鑫;杨东;鲁永玲;郑江2.野黄芩苷拮抗内毒素抑制人牙周膜细胞增殖作用的实验研究 [J], 杨宁;张莹;葛志华;王春艳3.升高高密度脂蛋白胆固醇（HDL-C）面临的挑战——升HDL-C药物的不同机制和HDL-C升高的疗效评价 [J], 曲鹏;王虹艳4.升高高密度脂蛋白胆固醇(HDL-C)面临的挑战——升HDL-C药物的不同机制和HDL-C升高的疗效评价 [J], 曲鹏; 王虹艳5.抗内毒素IgY体外拮抗内毒素效应的实验研究 [J], 李强;张雅萍因版权原因，仅展示原文概要，查看原文内容请购买。
高密度蛋白质检查结果0.59 -回复“高密度蛋白质检查结果0.59”是什么意思？高密度蛋白质(HDL)是一种与心血管健康密切相关的血液脂质，也被称为“好胆固醇”。
它起着清除血管内的低密度脂蛋白质(LDL)和其他有害物质的作用，降低动脉粥样硬化的风险。
检查结果0.59可能指的是HDL水平的数值，但需要明确单位和参考范围。
在本文中，我们将探讨HDL的重要性，如何提高HDL水平以及其与心血管健康的关系。
高密度蛋白质（HDL）在我们的身体中起着至关重要的作用。
它是一种蛋白质颗粒，可以通过血液循环从动脉壁中取走剩余的胆固醇。
HDL的主要功能是将胆固醇从动脉粥样硬化斑块中清除出来，并将其运送回肝脏以进行代谢和排泄。
HDL水平的测量通常通过血液检测来完成。
通常情况下，HDL水平在40-60 mg/dL或1.04-1.55 mmol/L之间被认为是正常的。
此时，较高的HDL水平通常被视为较好的健康指标。
那么，如果你的HDL水平为0.59，你应该如何应对呢？首先，我们需要了解为什么你的HDL水平较低。
有几个因素可能导致HDL水平下降，包括不良的生活习惯，基因遗传和一些慢性疾病。
首先，我们来看看生活习惯如何影响HDL水平。
吸烟、饮酒过量、饮食不健康以及缺乏运动都可能导致HDL水平的下降。
吸烟会损害血管内皮细胞，对HDL的生产和功能产生不利影响。
饮酒过量会影响肝脏的代谢功能，从而减少HDL的产生和清除能力。
其次，基因遗传也可能影响HDL水平。
某些人可能天生HDL水平较低，这取决于他们的遗传基因。
这并不意味着他们注定要患上心血管疾病，但他们需要更加关注其他心血管健康因素。
最后，一些慢性疾病也可能导致HDL水平下降。
例如，糖尿病、肾脏疾病和甲状腺功能低下都可能对HDL水平产生不利影响。
既然我们了解了HDL水平下降的原因，接下来我们将探讨一些提高HDL 水平的方法。
首先，你可以尝试改善生活习惯。
戒烟、减少饮酒量并遵循健康饮食和运动计划。
龙源期刊网 他汀类药物使用误区作者：任金姝来源：《百姓生活》2018年第10期误区一：血脂正常不宜应用他汀类药物治疗研究表明，心脑血管疾病一二级预防中他汀类药物必不可少。
一些医生常以血脂化验作为是否应用调脂药物的标准，认为血脂指标正常则不宜应用调脂药物。
正常的血脂检查指标并不适用于所有患者，不同疾病人群，如伴有或不伴有心脑血管危险因素的人群，其血脂标准水平不同。
以低密度脂蛋白胆固醇（LDL-C）为例，健康人应保持在4.6 mmol/L以下，高血压应低于3.38 mmol/L，冠心病或心肌梗死患者应保持在2.6 mmol/L 以下。
因此，对正常人而言正常范围的血脂，对糖尿病、冠心病或心肌梗死患者来讲已属高值，应予以他汀类药物进行调脂治疗。
由于他汀类药物可以逆转动脉粥样硬化斑块的作用，目前强调在以下情况，不论患者血脂水平如何，均应强化他汀类药物治疗：①临床已有冠心病；②有冠心病等危症；③有多种代谢危险因素，如代谢综合征。
误区二：他汀类药物仅适用于心脑血管疾病二级预防英国发表的HPS研究（心脏保护研究），涉及20536例冠心病或心血管高危人群。
研究发现，不论患者基础LDL-C水平如何（包括LDL-C多项研究表明，在心脑血管疾病患者中50%的患者存在血脂异常，服用他汀类药物对减少心脑血管事件比降低LDL-C更明显，无疑是他汀类药物多向效性非调脂作用的结果，也说明他汀类药物干预的不仅是血脂水平，更多干预的是心脑血管疾病危险水平。
误区三：在调脂治疗时常以总胆固醇降低作为治疗目标血清总胆固醇（TC）是指血清中各类脂蛋白所含胆固醇（包括游离胆固醇和胆固醇酯）的总和。
通常情况下，TC=LDL-C+ HDL-C（高密度脂蛋白膽固醇）+ VLDL-C（极低密度脂蛋白胆固醇）。
低密度脂蛋白（LDL）是致动脉粥样硬化的基本因素，代谢相对较简单，胆固醇约占LDL 重量的50%，故目前认为，LDL-C浓度基本能反映血液LDL总量。
高密度脂蛋白胆固醇0.67：解读、影响与提升策略一、引言血脂水平是衡量人体健康状况的重要指标之一，其中高密度脂蛋白胆固醇（HDL-C）的作用尤为突出。
HDL-C可以帮助清除血管壁的胆固醇，降低动脉硬化的风险。
然而，当HDL-C水平偏低，如0.67mmol/L时，可能会对健康产生不利影响。
本文将详细解读HDL-C 0.67的含义，探讨其可能的影响，并提供提升HDL-C水平的策略。
二、HDL-C 0.67的含义HDL-C的正常范围通常为1.03-1.55 mmol/L，因此，HDL-C 0.67属于偏低水平。
这意味着个体清除血管壁胆固醇的能力可能下降，从而增加患心血管疾病的风险。
了解HDL-C 0.67的含义有助于我们更好地评估个体的心血管健康状况，并采取相应措施进行改善。
三、HDL-C 0.67的可能影响1. 增加患心血管疾病的风险：HDL-C水平偏低可能导致血管壁胆固醇堆积，加速动脉硬化的发展，从而增加患冠心病、心肌梗死等心血管疾病的风险。
2. 影响其他血脂指标：HDL-C与其他血脂指标如低密度脂蛋白胆固醇（LDL-C）、甘油三酯等密切相关。
HDL-C水平偏低可能导致其他血脂指标异常，进一步影响心血管健康。
3. 不利于糖尿病患者的血糖控制：糖尿病患者本身容易出现血脂异常，HDL-C水平偏低可能加重血脂紊乱，不利于血糖控制。
4. 影响认知功能：研究表明，HDL-C水平偏低可能与认知功能下降、老年痴呆等疾病有关。
四、提升HDL-C水平的策略1. 改善饮食习惯：增加富含可溶性纤维的食物摄入，如燕麦、豆类、水果和蔬菜等，有助于提高HDL-C水平。
同时，减少饱和脂肪和反式脂肪的摄入，以降低LDL-C水平。
2. 增加体育锻炼：定期进行有氧运动，如慢跑、游泳和骑自行车等，可以提高HDL-C水平。
建议每周进行至少150分钟的中等强度有氧运动或75分钟的高强度有氧运动。
3. 戒烟限酒：吸烟和过量饮酒都会导致HDL-C水平下降。
脂血的判断标准"脂血"通常是指血液中脂质（如胆固醇和甘油三酯）含量异常增高的情况，可能会增加患心血管疾病的风险。
脂血的判断标准通常涉及测量血液中不同类型脂质的含量，并根据特定的参考范围来确定是否存在异常。
以下是常见的脂血判断标准：总胆固醇（Total Cholesterol，TC）：总胆固醇是血液中所有胆固醇的总和。
一般来说，总胆固醇水平应该控制在特定的范围内。
通常，总胆固醇水平的评价标准如下：理想水平：小于200毫克/分升（mg/dL）边缘高：200-239 mg/dL高风险：大于240 mg/dL低密度脂蛋白胆固醇（Low-density lipoprotein cholesterol，LDL-C）：LDL-C 被称为“坏胆固醇”，因为高水平的LDL-C与心血管疾病的风险增加相关。
通常，LDL-C水平的评价标准如下：理想水平：小于100 mg/dL边缘高：100-129 mg/dL高风险：大于130 mg/dL高密度脂蛋白胆固醇（High-density lipoprotein cholesterol，HDL-C）：HDL-C被称为“好胆固醇”，因为它有助于清除动脉中的胆固醇。
通常，HDL-C水平的评价标准如下：低水平：男性小于40 mg/dL，女性小于50 mg/dL正常水平：男性大于40 mg/dL，女性大于50 mg/dL甘油三酯（Triglycerides，TG）：甘油三酯是血液中最常见的脂质之一，高水平的甘油三酯与心血管疾病的风险增加相关。
通常，甘油三酯水平的评价标准如下：理想水平：小于150 mg/dL边缘高：150-199 mg/dL高风险：大于200 mg/dL这些标准可能会根据个体的健康状况、年龄、性别和其他因素而有所不同。
建议在评估脂血时，应该综合考虑多种指标，并结合个体的整体健康状况和心血管疾病的其他危险因素进行评估。
如果有脂血异常的迹象，建议咨询医疗专业人士进行详细评估和治疗建议。
HDL Cholesterol Efflux Does Not Predict Cardiovascular Risk in Hemodialysis PatientsChantal Kopecky,*Sanam Ebtehaj,†Bernd Genser,‡§|Christiane Drechsler,¶**Vera Krane,¶** Marlies Antlanger,*Johannes J.Kovarik,*Christopher C.Kaltenecker,*Mojtaba Parvizi,††Christoph Wanner,¶**Thomas Weichhart,‡‡Marcus D.Säemann,*and Uwe J.F.Tietge†*Department of Internal Medicine III,Division of Nephrology and Dialysis and‡‡Institute of Medical Genetics,Medical University of Vienna,Vienna,Austria;†Department of Pediatrics,Center for Liver,Digestive,and Metabolic Diseases and ††Department of Pathology and Medical Biology,University of Groningen,University Medical Center Groningen, Groningen,The Netherlands;‡BGStats Consulting,Vienna,Austria;§Mannheim Institute of Public Health,Social and Preventive Medicine,Medical Faculty Mannheim,Heidelberg University,Heidelberg,Germany;|Institute of Public Health,Federal University of Bahia,Salvador,Brazil;and¶Division of Nephrology,Department of Medicine1and**Comprehensive Heart Failure Centre,University of Würzburg,Wurzburg,GermanyABSTRACTThe cardioprotective effect of HDL is thought to be largely determined by its cho-lesterol efflux capacity,which was shown to inversely correlate with atheroscleroticcardiovascular disease in populations with normal kidney function.Patients withESRD suffer an exceptionally high cardiovascular risk not fully explained by tradi-tional risk factors.Here,in a post hoc analysis in1147patients with type2diabetesmellitus on hemodialysis who participated in the German Diabetes Dialysis Study(4D Study),we investigated whether the HDL cholesterol efflux capacity is predic-tive for cardiovascular risk.Efflux capacity was quantified by incubating human mac-rophage foam cells with apoB-depleted serum.During a median follow-up of4.1years,423patients reached the combined primary end point(composite of cardiacdeath,nonfatal myocardial infarction,and stroke),410patients experienced cardiacevents,and561patients died.Notably,in Cox regression analyses,we found noassociation of efflux capacity with the combined primary end point(hazard ratio[HR],0.96;95%confidence interval[95%CI],0.88to1.06;P=0.42),cardiac events(HR,0.92;95%CI,0.83to1.02;P=0.11),or all-cause mortality(HR,0.96;95%CI,0.88to1.05;P=0.39).In conclusion,HDL cholesterol efflux capacity is not a prognosticcardiovascular risk marker in this cohort of patients with diabetes on hemodialysis.J Am Soc Nephrol28:ccc–ccc,2016.doi:10.1681/ASN.2016030262Plasma levels of HDL cholesterol(HDL-C) are inversely correlated with the risk of atherosclerotic cardiovascular disease (CVD)in large population studies,1but recentfindings called the usefulness of static HDL-C measurements as a predic-tive biomarker into question.2–5Rather, determining functional properties of the HDL particle represents an emerging concept in cardiovascular research.6,7Ac-cordingly,promoting HDL-C efflux from macrophage foam cells plays a cen-tral role and is regarded crucial in reversecholesterol transport(RCT).8,9In popu-lations with normal kidney function,alower cholesterol efflux capacity was as-sociated with increased cardiovascularmorbidity and mortality,even indepen-dent of HDL-C concentrations.10,11Patients with ESRD represent a popu-lation with an excessively increased cardio-vascular risk,12which is even potentiatedby diabetes as a frequent comorbidity.13Importantly,measurements of HDL-Clevels have a rather limited predictivevalue in these patients,14–16making itconceivable that alterations in HDL func-tion represent an underlying causativecontributor to atherosclerotic risk.How-ever,to date,the potential importance ofthis novel concept for patients withESRD has not been assessed.Therefore,we investigated in this work if cholesterolefflux as a key metric of HDL function-ality is predictive for cardiovascular riskand overall mortality in patients withESRD participating in the German Dia-betes Dialysis Study(4D Study),a pro-spective trial exploring the efficacy ofatorvastatin treatment in subjects withtype2diabetes mellitus on hemodialysis.Received March7,2016.Accepted July17,2016.C.K.and S.E.,and M.D.S.and U.J.F.T.contributedequally to this work.Published online ahead of print.Publication dateavailable at .Correspondence:Dr.Uwe J.F.Tietge,Departmentof Pediatrics,Center for Liver,Digestive,andMetabolic Diseases,University Medical CenterGroningen,Hanzeplein1,9713GZ Groningen,TheNetherlands.Email:u_tietge@Copyright©2016by the American Society ofNephrologyJ Am Soc Nephrol28:ccc–ccc,2016ISSN:1046-6673/2803-ccc1In this post hoc analysis of the4D Study,we measured HDL-C efflux in 1147patients who were divided into ter-tiles on the basis of cholesterol efflux ca-pacity:first tertile,median=0.73 (interquartile range[IQR],0.67–0.77); second tertile,median=0.89(IQR,0.86–0.94);and third tertile,median=1.08 (IQR,1.02–1.20).Baseline characteristics of the study participants according to tertiles of cholesterol efflux capacity are shown in Table1.The proportion of men decreased significantly with in-creasing HDL efflux capacity along with the levels of the inflammatory pro-teins C-reactive protein(CRP)and HDL–bound serum amyloid A(SAA[HDL]).Higher cholesterol efflux was paralleledby increased plasma total cholesterol,LDL cholesterol(LDL-C),HDL-C,apoA-I,albumin,apoC-III,symmetricdimethylarginine,and carbamylated al-bumin.Of note,patients in thefirsttertile had a shorter duration of hemo-dialysis treatment and lower phosphatelevels.There was no difference in age,bodymass index,systolic BP,hypertension,or previous history of CVD throughoutthe tertiles.We next determined clinical parame-ters correlated with cholesterol effluxcapacity in patients on dialysis(Supple-mental Table1)and found strong posi-tive correlations with plasma HDL-C(r=0.25;P,0.001),apoA-I(r=0.26;P,0.001),and albumin(r=0.16;P,0.001).There were weaker correla-tions with LDL-C(r=0.10;P=0.001)and dialysis duration(r=0.10;P=0.001).Of note,there was no significant rela-tion between cholesterol efflux andthe inflammation markers CRP andSAA(HDL).During a median follow-up of4.1years,a total of423study participantsreached the combined primary end point(composite of cardiac death,nonfatalmyocardial infarction,and stroke),410experienced cardiac events(cardiacdeath and nonfatal myocardial infarc-tion),and561died(all-cause mortality).Table1.Baseline characteristics of the study participants according to tertiles of cholesterol efflux capacity Parameter Tertile1,n=383Tertile2,n=382Tertile3,n=382P ValueCholesterol efflux capacity0.73[0.67–0.77]0.89[0.86–0.94] 1.08[1.02–1.20]Age,yr66.7(8.2)66.2(8.4)66.0(8.2)0.49 Body mass index,kg/m227.5(4.7)27.7(5.0)27.4(4.8)0.72 Duration of diabetes,yr17.8(8.2)18.4(8.9)18.1(8.5)0.62 Duration of dialysis,mo 5.5[3.2–10.4] 5.6[2.6–11.8] 6.7[3.4–12.2]0.03 Men,n(%)233(61.0)207(54.2)188(49.1)0.004 Nonsmoker,n(%)213(55.8)234(61.3)235(61.4)0.41 History,n(%)Arrhythmia81(21.2)69(18.1)62(16.2)0.20 Congestive heart failure166(43.5)130(34.0)115(30.0),0.001 Stroke/TIA68(17.8)66(17.3)68(17.8)0.98 Peripheral vascular disease174(45.6)166(43.5)174(45.4)0.81 MI/CABG/PTCA/CAD128(33.5)106(27.8)109(28.5)0.17 Hypertension336(88.0)341(89.3)341(89.0)0.83 Systolic BP,mmHg144.4(23.2)146.5(20.9)146.4(21.8)0.32 Diastolic BP,mmHg74.6(10.7)76.3(10.5)76.6(11.4)0.02 Total cholesterol,mg/dl209.8(42.0)221.5(41.8)226.9(40.8),0.001 Triglycerides,mg/dl219.5[149.0–345.0]227.5[158.0–332.0]210.0[139.0–298.0],0.01 LDL-C,mg/dl119.1(27.9)126.9(28.9)131.9(30.2),0.001 HDL-C,mg/dl31.2(9.9)35.6(12.5)42.3(15.6),0.001 C-reactive protein,mg/L 6.2[3.1–13.4] 5.4[2.2–11.1]7.1[2.6–11.1]0.01 Albumin,g/dl 3.8(0.3) 3.8(0.3) 3.9(0.3),0.001 Hemoglobin,g/dl10.9(1.4)10.9(1.3)10.9(1.3)0.90 Hemoglobin A1c,% 6.7(1.3) 6.7(1.3) 6.8(1.2)0.69 Phosphate,mg/dl 5.8(1.7) 6.1(1.6) 6.2(1.6),0.01 apoA-I,mg/dl115.8(19.9)125.5(20.0)137.6(25.5),0.001 SAA(HDL) 6.7[3.0–13.9] 5.6[2.7–12.3] 5.3[2.9–10.2]0.01 SP-B(HDL)7.3[4.0–13.0] 6.6[3.5–13.7] 5.6[3.1–11.7]0.17 apoC-III,mg/dl19.3(9.5)20.8(10.0)20.9(9.0)0.03 apoC-II,mg/dl 6.0(3.1) 6.5(3.3) 6.4(2.7)0.07 ADMA0.9(0.2)0.9(0.2)0.9(0.2)0.37 SDMA 2.5(0.8) 2.6(0.8) 2.6(0.8)0.03 Carbamylated albumin0.6(0.3)0.6(0.3)0.7(0.3),0.001 Data shown are means(SDs)or medians[IQRs]if not indicated otherwise.P values for comparisons of groups were calculated from ANOVA models(for continuous variables)or logistic regression models(for categorical variables).TIA,transitory ischemic attack;MI,myocardial infarction;CABG,coronary artery bypass grafting surgery;PTCA,percutaneous transluminal coronary angioplasty;CAD,coronary artery disease;SP-B(HDL),HDL–bound surfactant protein B;ADMA,asymmetric dimethylarginine;SDMA,symmetric dimethylarginine.2Journal of the American Society of Nephrology J Am Soc Nephrol28:ccc–ccc,2016In an univariate Cox regression analysis examining the prognostic effect of base-line cholesterol ef flux capacity for selected end points (Figure 1),we found no association with cholesterol ef flux and the combined primary end point (hazard ratio [HR]per 1-SD increase,0.96;95%con fidence interval [95%CI],0.88to 1.06;P =0.42),all cardiac events combined (HR per 1-SD increase,0.92;95%CI,0.83to 1.02;P =0.11),or all-cause mortality (HR per 1-SD in-crease,0.96;95%CI,0.88to 1.05;P =0.39).Multivariate Cox regression analyses with additional adjustment for a number of relevant clinical param-eters (Table 2)further strengthened the conclusion that cholesterol ef flux capac-ity was not associated with the risk for cardiovascular events or mortality in pa-tients on hemodialysis.The respective Cox models according to tertiles of cho-lesterol ef flux are shown in Supplemen-tal Table 2.Next,participants were also strati fied according to event occurrence (Supple-mental Table 3).Baseline HDL-C ef flux,total cholesterol,and HDL-C levels were not different between patients who reached the de fined end points and those who did not.For all three analyzed end points,patients with an event during follow-up had a higher prevalence of preexisting CVD and longer diabetes duration as well as lower hemoglobin and phosphate levels.Notably,pa-tients who died displayed pronounced signs of wasting and in flammation in-dicated by higher age,lower body mass index,higher prevalence of cardiovas-cular complications,higher plasma LDL-C,and higher levels of CRP and SAA(HDL).Furthermore,we attempted to determine a potential role for cholesterol ef fluxcapacity in the treatment ef ficacy of atorvastatin in the 4D Study population.Interestingly,strati fied subgroup analy-sis by tertiles indicated a potential effect modi fication of atorvastatin on cardiac events (Supplemental Figure1),Figure 1.HDL cholesterol ef flux capacity is not associated with end points.Kaplan –Meier curves according to tertiles of cholesterol ef flux capacity.Prognostic effect of cholesterol ef flux capacity on (A)combined primary end point (composite of cardiac death,nonfatal myocardial infarction,and stroke),(B)cardiac events combined,and (C)all-cause mortality.J Am Soc Nephrol 28:ccc –ccc ,2016Cholesterol Ef flux in the 4D Study 3although the overall effect was not sig-nificant(P=0.19).In patients with the lowest cholesterol efflux capacity, atorvastatin reduced the risk for all car-diac events combined(HR per1-SD in-crease,0.66;95%CI,0.47to0.92;P=0.02), which remained significant after addi-tional adjustment with a number of rel-evant clinical parameters(Table3).By contrast,in the higher tertiles of choles-terol efflux,no differential effect of sta-tin treatment was observed.This post hoc analysis of the4D Study shows that HDL-C efflux capacity is not associated with cardiovascular events or mortality in a large and sufficiently pow-ered cohort of patients with diabetes and ESRD on hemodialysis.These data are consistent with our previous obser-vation that HDL-C efflux did not pre-dict all–cause or specific CVD mortality in kidney transplant recipients.In-triguingly,however,higher efflux was independently associated with graft sur-vival;thus,cholesterol efflux might represent a meaningful predictor of graft outcome.17Hence,our results extend previous observations that plasma HDL-C levels have little association with the risk of cardiovascular morbidity or mortality in ESRD18to the emerging area of HDL function studies.However,ourfindings are in apparent contrast to the prevailing view in the cardiovascularfield that,at least in cohorts with normal or only mildly impaired kidney function,the cholesterol efflux capacity of HDL might be an even stronger predictor for CVDrisk than the mere measurement of cir-culating levels of HDL-C or apoA-I.10,11Although it should be noted that not alldata on risk prediction by measuringcholesterol efflux are consistent withsuch a concept,19we do believe that spe-cific characteristics of patients withESRD affect the outcome of our study.Smaller cross–sectional studies carriedout in the setting of renal failure indi-cated several functional impairments ofHDL,which are not restricted to de-creased cholesterol efflux but affect itsanti–inflammatory,19antioxidative,20or endothelial health–promoting activi-ties21to a similar degree.Potential un-derlying reasons for the dysfunctionalHDL in kidney disease could be thehigh inflammatory and oxidative stressburden of ESRD that contributes to theexcessive cardiovascular risk and isaccelerated by the presence of diabe-tes.22,23In fact,certain modifications inthe protein composition of uremic HDLlinked to chronic systemic inflammationconceivably contribute to rendering theparticle ineffective in providing suffi-cient antiatherogenic protection.19,20Inthis respect,we have previously foundthat HDL of patients with ESRD haslost its anti-inflammatory property andeven acts proinflammatory as a directconsequence of enrichment with theacute–phase protein serum amyloid A.19Subsequently,we could show thathigh SAA(HDL)levels were predictiveof cardiac events in the4D Studypopulation.24Such data suggest that theprotein cargo on HDL might provideuseful biomarkers to predict clinicalevents.Another interesting outcome of ourstudy was a potential effect modificationof statin treatment.We found that ator-vastatin reduced the risk for all cardiacevents in patients of thefirst cholesterolefflux tertile.Given the general contro-versy of beneficial treatment effects ofstatins in patients on dialysis,25–27theobserved effect modification needs tobe viewed with caution,and it will becritical to validate our results in inde-pendent patient collectives.However,even after adjustment for a number ofrelevant confounders,this effect re-mained significant,indicating a poten-tial clinical relevance of our observation.Thus,our data suggest that cholesterolefflux capacity might be useful as a po-tential tool to identify subgroups of pa-tients with ESRD that could benefit fromstatin treatment.A potential limitation of our study isthat the patients already had a longhistory of diabetes and likely,also de-veloped CVD over a prolonged period oftime.Therefore,baseline cholesterol ef-flux may not fully reflect HDL effluxcapacity during follow-up.With respectto the efflux assay,our assay systemmainly differs in the choice of cell linefrom comparable studies in non-CKDcohorts.10,11Such studies used cholesterol–equilibrated murine J774cells with limitedbaseline expression of ABCA1,which onTable2.HRs for combined primary end point,all cardiac events combined,and all-cause mortality by cholesterol efflux capacityCombined Primary End Point,498Events All Cardiac Events Combined,534EventsAll-Cause Mortality,561EventsHR(95%CI)per 1-SD Increase P Value HR(95%CI)per1-SD IncreaseP Value HR(95%CI)per1-SD IncreaseP ValueModel10.96(0.88to1.06)0.420.92(0.83to1.02)0.110.96(0.88to1.05)0.39 Model20.96(0.88to1.05)0.380.92(0.82to1.03)0.150.98(0.90to1.06)0.54 Model30.89(0.73to1.09)0.270.77(0.62to0.95)0.020.91(0.76to1.08)0.26 Model40.98(0.91to1.06)0.640.94(0.85to1.04)0.23 1.00(0.95to1.06).0.99 Model50.98(0.91to1.05)0.550.94(0.85to1.04)0.220.99(0.94to1.05)0.85 Model60.98(0.91to1.05)0.560.94(0.85to1.04)0.220.99(0.94to1.05)0.83 Continuous Cox regression model to assess the prognostic effect of cholesterol efflux on selected end bined primary end point(composite of cardiac death,nonfatal myocardial infarction,and stroke).Model1:univariate;model2:adjusted for age and sex;model3:adjusted for age,sex,and CRP;model4: adjusted for traditional risk factors(age,sex,coronary artery disease,arrhythmia,transitory ischemic attack,congestive heart failure,peripheral vascular disease, smoking,systolic/diastolic BP,body mass index,albumin,phosphate,hemoglobin,hemoglobin A1c,and duration of dialysis);model5:adjusted for traditional risk factors,LDL-C,HDL-C,and apoA-I;and model6:adjusted for traditional risk factors,LDL-C,HDL-C,apoA-I,and CRP.4Journal of the American Society of Nephrology J Am Soc Nephrol28:ccc–ccc,2016induction with cAMP ,becomes the domi-nant ef flux pathway.In contrast,we used a human cell line that was loaded with cho-lesterol to re flect foam cells and in which all ef flux pathways are active.7These differ-ences might affect the results to a certain extent;however,it has to be noted that,at present,no gold standard or comparative studies are available for ef flux assays.In addition,albumin was shown to facilitate cholesterol ef flux 7;because in our cohort,plasma albumin levels were within the nor-mal range throughout the tertiles,we do not expect this parameter to have a major effect on the results but can also not for-mally exclude it.Furthermore,cholesterol ef flux,as evaluated in this study,does not take ESRD-related changes in cells and tis-sues into account,which also play a role in RCT.Here,speci fically increased ACAT-1activity in,for example,macrophages is worth mentioning.28,29In addition,modi-fications of SR-BI by reactive oxygen spe-cies,myeloperoxidase,and glycation occur that negatively affect its cholesterol uptake function.30Such alterations possibly lead to an even more substantial reduction in overall RCT in ESRD.In conclusion,our study is the first to investigate the predictive potential of cholesterol ef flux capacity in patients on dialysis.Remarkably,there was no associ-ation of this key metric of HDL function and cardiovascular outcomes in this spe-ci fic patient population.Nonetheless,we believe that our study signi ficantly con-tributes to clarify the role of HDL in ESRD and adds important information to the understanding of the underlying patho-physiology of CVD in ESRD.The ultimate clinical goal remains the identi fication of novel and reliable risk predictors for CVD in patients with ESRD that also offer the possibility to be in fluenced by targeted therapies.CONCISE METHODS Study ParticipantsThe design of the 4D Study has been described previously.25The 4D Study was a double –blind,randomized,multicenter trial including 1255patients with type 2diabetes mellitus who were 18–80years of age and had a previousduration of hemodialysis of ,2years.Patients were recruited between March of 1998and October of 2002and randomly assigned to receive daily treatment with 20mg atorvastatin (n =619)or placebo (n =636).Participants were followed up at 4weeks and every 6months after randomization.At each follow-up visit,information about any suspected end point or serious adverse event was recorded.The study was approved by the local ethics com-mittees and performed according to the Dec-laration of Helsinki,and informed consent was obtained from all participants.Laboratory ProceduresHDL cholesterol ef flux capacity was determined from THP-1macrophages toward apoB-depleted plasma as acceptor following a previously re-ported protocol.17Brie fly,THP-1human mono-cytes (American T ype Culture Collection,Manassas,V A)were seeded in 48-well plates in RPMI 1640Glutamax Medium (Gibco,Carlsbad,CA)containing 10%FBS and penicillin (100U/ml)/streptomycin (100m g/ml)and differenti-ated into macrophages with 100nM phorbol myristate acetate for 24hours.Then,macro-phages were loaded for 24hours with acetylated LDL (50m g protein/ml)and 1m Ci/ml 3H cho-lesterol (PerkinElmer,Waltham,MA)followed by overnight equilibration with RPMI 1640Glutamax Medium containing 2%BSA.Thereafter,cells were washed with PBS,and 2%of individual apoB –depleted plasma sam-ples was added in RPMI 1640Glutamax Me-dium containing penicillin/streptomycin.After 5hours of ef flux,the medium was col-lected and centrifuged in a tabletop centrifuge (Hettich,Tuttlingen,Germany)for 5minutes at 10,000rpm to pellet cellular debris,and radioactivity was determined in an aliquot by liquid scintillation counting (Packard 1600CA Tri-Carb;Packard,Meriden,CT).To the cells,0.1M NaOH was added for at least 30minutes,and then,radioactivity re-maining in the cells was determined.Choles-terol ef flux was calculated as the percentage of radiolabel recovered in the medium related to the total added dose of radioactivity (counts from the medium added to counts from cells).Values obtained from negative control cells without added apoB –depleted patient plasma were subtracted to correct for unspeci fic ef-flux.Finally,values were normalized to a plasma pool from healthy controls present on every plate.Thus,values given for ef fluxT a b l e 3.C o x r e g r e s s i o n m o d e l s a s s e s s i n g t r e a t m e n t e f fic a c y o f a t o r v a s t a t i n o n a l l c a r d i a c e v e n t s c o m b i n e d s t r a t i fie d b y t e r t i l e s o f c h o l e s t e r o l e f flu xM o d e l 1M o d e l 2M o d e l 3M o d e l 4M o d e l 5H R (95%C I )P V a l u e H R (95%C I )P V a l u e H R (95%C I )P V a l u e H R (95%C I )P V a l u eH R (95%C I )P V a l u e T e r t i l e 10.66(0.47t o 0.92)0.020.65(0.47t o 0.92)0.010.68(0.49t o 0.94)0.020.70(0.50t o 0.98)0.040.70(0.50t o 0.97)0.03T e r t i l e 20.85(0.61t o 1.19)0.340.85(0.61t o 1.18)0.330.85(0.61t o 1.18)0.330.85(0.61t o 1.18)0.320.85(0.61t o 1.18)0.33T e r t i l e 30.85(0.56t o 1.27)0.420.84(0.56t o 1.26)0.400.70(0.48t o 1.02)0.070.69(0.47t o 1.01)0.060.69(0.47t o 1.01)0.06M o d e l 1:u n i v a r i a t e ;m o d e l 2:a d j u s t e d f o r a g e a n d s e x ;m o d e l 3:a d j u s t e d f o r t r a d i t i o n a l r i s k f a c t o r s (a g e ,s e x ,c o r o n a r y a r t e r y d i s e a s e ,a r r h y t h m i a ,t r a n s i e n t i s c h e m i c a t t a c k ,c o n g e s t i v e h e a r t f a i l u r e ,p e r i p h e r a l v a s c u l a r d i s e a s e ,s m o k i n g ,s y s t o l i c /d i a s t o l i c B P ,b o d y m a s s i n d e x ,a l b u m i n ,p h o s p h a t e ,h e m o g l o b i n ,h e m o g l o b i n A 1c ,a n d d u r a t i o n o f d i a l y s i s );m o d e l 4:a d j u s t e d f o r t r a d i t i o n a l r i s k f a c t o r s ,L D L -C ,H D L -C ,a n d a p o A -I ;a n d m o d e l 5:a d j u s t e d f o r t r a d i t i o n a l r i s k f a c t o r s ,L D L -C ,H D L -C ,a p o A -I ,a n d C R P .J Am Soc Nephrol 28:ccc –ccc ,2016Cholesterol Ef flux in the 4D Study5do not have a specific unit.All determinations were carried out in duplicates at the same time using the same reagents to reduce variation caused by different assay conditions.The intra-assay CV of this method is5.4%,and the interassay CV is7.9%.End PointsFor our post hoc analysis,we evaluated the following predefined and centrally adjudi-cated outcome measures:(1)combined pri-mary end point(composite of cardiac death, nonfatal myocardial infarction,and stroke), (2)all cardiac events combined(cardiac death and nonfatal myocardial infarction), and(3)all-cause mortality.Statistical AnalysesWe examined characteristics of subgroups defined by tertiles of cholesterol efflux by calculating descriptive statistics(means and SDs for continuous variables and frequency tables for categorical variables).We compared the distribution of important cardiovascular parameters across tertiles by using ANOVA (for continuous variables)or chi-squared tests(for categorical variables).Furthermore, we conducted a correlation analysis calculat-ing Pearson correlation coefficients to in-vestigate which clinical parameters were correlated with cholesterol efflux capacity in patients on dialysis.We used time to event analysis(extended Cox regression model allowing for multiple events)aimed to(1) evaluate the effect of cholesterol efflux on end point occurrence,and(2)investigate the effect of cholesterol efflux on the efficacy of atorvastatin.For1,we conducted a pooled analysis in both randomization groups, including a dummy variable for randomiza-tion group and efflux capacity as continuous covariates,standardized by the sample SD. For2,we conducted efficacy analysis calcu-lating HRs for atorvastatin versus placebo stratified by efflux tertiles.For both analyses, we conducted sensitivity analysis,fitting dif-ferent models that each included different covariates:model1:no additional covariate adjustment;model2:adjusted for age and sex;model3:adjusted for age,sex,and CRP;model4:adjusted for traditional risk factors(age,sex,coronary artery disease,ar-rhythmia,transitory ischemic attack,conges-tive heart failure,peripheral vascular disease, smoking,systolic/diastolic BP,body mass index,albumin,phosphate,hemoglobin,he-moglobin A1c,and duration of dialysis);model5:adjusted for traditional risk factors,LDL-C,HDL-C,and apoA-I;and model6:adjusted for traditional risk factors,LDL-C,HDL-C,apoA-I,and CRP.All statistical analyses were performedusing the statistical software package STATA(StataCorp.2011,Stata Statistical Software:Release13;StataCorp.,College Station,TX).ACKNOWLEDGMENTSThis work was supported by a grant from TheNetherlands Organization for Scientific Re-search(VIDI Grant917-56-358to U.J.F.T.).DISCLOSURESNone.REFERENCES1.Gordon DJ,Probstfield JL,Garrison RJ,Neaton JD,Castelli WP,Knoke JD,JacobsDR Jr.,Bangdiwala S,Tyroler HA:High-density lipoprotein cholesterol and cardio-vascular disease.Four prospective Americanstudies.Circulation79:8–15,19892.van Capelleveen JC,Bochem AE,MotazackerMM,Hovingh GK,Kastelein JJ:Genetics ofHDL-C:A causal link to atherosclerosis?CurrAtheroscler Rep15:326,20133.Toth PP,Barter PJ,Rosenson RS,Boden WE,Chapman MJ,Cuchel M,D’Agostino RB Sr.,Davidson MH,Davidson WS,Heinecke JW,Karas RH,Kontush A,Krauss RM,Miller M,Rader DJ:High-density lipoproteins:A con-sensus statement from the National LipidAssociation.J Clin Lipidol7:484–525,20134.Ray K,Wainwright NW,Visser L,Witteman J,Breteler M,Ambegaonkar B,Hofman A,Stricker B,Wareham N,Khaw KT,Sandhu M:Changes in HDL cholesterol and cardiovas-cular outcomes after lipid modification ther-apy.Heart98:780–785,20125.Voight BF,Peloso GM,Orho-Melander M,Frikke-Schmidt R,Barbalic M,Jensen MK,Hindy G,Hólm H,Ding EL,Johnson T,Schunkert H,Samani NJ,Clarke R,HopewellJC,Thompson JF,Li M,Thorleifsson G,Newton-Cheh C,Musunuru K,Pirruccello JP,Saleheen D,Chen L,Stewart A,Schillert A,Thorsteinsdottir U,Thorgeirsson G,Anand S,Engert JC,Morgan T,Spertus J,Stoll M,Berger K,Martinelli N,Girelli D,McKeownPP,Patterson CC,Epstein SE,Devaney J,Burnett MS,Mooser V,Ripatti S,Surakka I,Nieminen MS,Sinisalo J,Lokki ML,Perola M,Havulinna A,de Faire U,Gigante B,IngelssonE,Zeller T,Wild P,de Bakker PI,Klungel OH,Maitland-van der Zee AH,Peters BJ,de BoerA,Grobbee DE,Kamphuisen PW,DeneerVH,Elbers CC,Onland-Moret NC,HofkerMH,Wijmenga C,Verschuren WM,Boer JM,van der Schouw YT,Rasheed A,Frossard P,Demissie S,Willer C,Do R,Ordovas JM,Abecasis GR,Boehnke M,Mohlke KL,DalyMJ,Guiducci C,Burtt NP,Surti A,GonzalezE,Purcell S,Gabriel S,Marrugat J,Peden J,Erdmann J,Diemert P,Willenborg C,KönigIR,Fischer M,Hengstenberg C,Ziegler A,Buysschaert I,Lambrechts D,Van de Werf F,Fox KA,El Mokhtari NE,Rubin D,Schrezenmeir J,Schreiber S,Schäfer A,Danesh J,Blankenberg S,Roberts R,McPherson R,Watkins H,Hall AS,Overvad K,Rimm E,Boerwinkle E,Tybjaerg-Hansen A,Cupples LA,Reilly MP,Melander O,Mannucci PM,Ardissino D,Siscovick D,Elosua R,Stefansson K,O’Donnell CJ,Salomaa V,Rader DJ,Peltonen L,SchwartzSM,Altshuler D,Kathiresan S:Plasma HDLcholesterol and risk of myocardial infarction:A mendelian randomisation ncet380:572–580,20126.Heinecke JW:The not-so-simple HDL story:A new era for quantifying HDL and cardio-vascular risk?Nat Med18:1346–1347,20127.Triolo M,Annema W,Dullaart RP,Tietge UJ:Assessing the functional properties of high-density lipoproteins:An emerging concept incardiovascular research.Biomarkers Med7:457–472,20138.Annema W,Tietge UJ:Regulation of reversecholesterol transport-a comprehensive ap-praisal of available animal studies.NutrMetab(Lond)9:25,20129.Khera AV,Rader DJ:Future therapeutic di-rections in reverse cholesterol transport.CurrAtheroscler Rep12:73–81,201010.Rohatgi A,Khera A,Berry JD,Givens EG,Ayers CR,Wedin KE,Neeland IJ,Yuhanna IS,Rader DR,de Lemos JA,Shaul PW:HDLcholesterol efflux capacity and incident car-diovascular events.N Engl J Med371:2383–2393,201411.Khera AV,Cuchel M,de la Llera-Moya M,Rodrigues A,Burke MF,Jafri K,French BC,Phillips JA,Mucksavage ML,Wilensky RL,Mohler ER,Rothblat GH,Rader DJ:Choles-terol efflux capacity,high-density lipoproteinfunction,and atherosclerosis.N Engl J Med364:127–135,201112.Ortiz A,Covic A,Fliser D,Fouque D,Goldsmith D,Kanbay M,Mallamaci F,MassyZA,Rossignol P,Vanholder R,Wiecek A,Zoccali C,London GM;Board of theEURECA-m Working Group of ERA-EDTA:Epidemiology,contributors to,and clinicaltrials of mortality risk in chronic kidney failure.Lancet383:1831–1843,201413.Jardine MJ,Hata J,Woodward M,PerkovicV,Ninomiya T,Arima H,Zoungas S,Cass A,6Journal of the American Society of Nephrology J Am Soc Nephrol28:ccc–ccc,2016。
