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2022.10.30吉林
慢性肾脏病高甘油三酯血症管理专家共识专家组
通信作者：梅长林，上海长征医院肾脏病科，海军军医大学，上海200003，Email：chlmei1954@126.com
【关键词】高甘油三酯血症；慢性肾脏病；治疗；管理；专家共识
DOI：10.3760/cma.j.cn441217-20220217-00111
1.CKD患者发生HTG原因：①脂蛋白脂酶活性受抑制，引起甘油三酯水平升高[12-13]；②极低密度脂蛋白受体表达下调引起极低密度脂蛋白清除下降[5,13]；③参与脂肪酸生物合成的关键酶，包括乙酰辅酶A羧化酶和脂肪酸合成酶表达增加，导致脂肪酸合成增多[13]。
2.HTG在CKD中的致病机制[14-16]：①甘油三酯在肾脏沉积，包括在足细胞、系膜细胞和近曲小管上皮细胞的脂质沉积，引起脂质肾毒性；②脂质沉积刺激足细胞脱离和凋亡、系膜细胞增生及肾小球硬化；③足细胞损伤使与白蛋白结合的游离脂肪酸滤过进入近曲小管并被重吸收，游离脂肪酸在线粒体氧化，使活性氧增加，导致肾小管细胞损伤和凋亡；④富含甘油三酯脂蛋白还可通过NLR家族蛋白3炎症体介导炎症。
4.限制饮酒：中等量饮酒（含30g乙醇）对基线甘油三酯水平正常者的甘油三酯水平影响不大，甘油三酯水平变化（约15%）通常是暂时的[43]。但对于HTG患者，即使少量饮酒也会使患者甘油三酯水平进一步升高[30]。长期过量饮酒会导致空腹甘油三酯升高[43]，而甘油三酯水平严重升高会增加患胰腺炎的风险[20]。有研究报道，轻中度饮酒对CKD患者可能存在益处[47]，但由于饮酒可能对健康造成其他危害，建议CKD患者少饮酒或不饮酒。
尽管健康的饮食和生活方式对降低甘油三酯水平效果显著，但鉴于CKD患者病情的复杂情况，治疗性生活方式干预的具体方式仍需要根据实际情况进行调整，且长期依从性差是一个严重问题[48]。我们提倡强化生活方式干预，对于生活方式干预后甘油三酯水平仍高的患者，需要进行药物干预。
1.贝特类药物：贝特类药物是过氧化物酶体增殖物激活受体α（peroxisomeproliferator-activatedreceptorα，PPARα）激动剂，通过激活PPARα和脂蛋白脂酶而降低血清甘油三酯水平、升高HDL胆固醇水平[20]。贝特类药物在肾脏代谢并主要通过肾脏清除，易导致血清肌酐升高[54]。其禁忌证包括严重肾功能不全、透析和活动性肝病等；与他汀类药物联用时出现肌病和横纹肌溶解症风险增加，特别是老年、糖尿病和肾衰竭患者[9,55]。在CKD3期患者的临床试验表明，贝特类药物（非诺贝特、苯扎贝特）联用他汀类药物可降低CKD患者甘油三酯水平38%左右[56]，降低心血管事件风险27%～40%[57-59]，但同时eGFR下降发生率增加约9%[56]。荟萃分析显示，与他汀类单药治疗相比，他汀类联用贝特类药物增加肾功能损害风险[60]。贝特类新药（佩玛贝特）主要经肝脏代谢，具有良好的肾脏安全性，在降低CKD伴HTG患者甘油三酯水平45.9%的同时，不加速eGFR下降[61]，但在我国尚未上市。
特殊CKD人群包括肾病综合征、IgA肾病、糖尿病肾脏疾病（diabetickidneydisease，DKD）、CKD4～5期非透析、血液透析、腹膜透析和肾移植等患者，这些患者血脂代谢异常谱有所不同，见表3[80-81]。
慢性肾脏病高甘油三酯血症管理专家共识专家组专家组组长：梅长林专家组成员（按姓名汉语拼音排序）：
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