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小高密度脂蛋白亚类与慢性肾脏病死亡风险的关联

Association of Small HDL Subclasses with Mortality Risk in Chronic Kidney Disease.

作者信息

Stadler Julia T, Borenich Andrea, Pammer Anja, Emrich Insa E, Habisch Hansjörg, Madl Tobias, Heine Gunnar H, Marsche Gunther

机构信息

Division of Pharmacology, Otto Loewi Research Center for Vascular Biology, Immunology and Inflammation, Medical University of Graz, Neue Stiftingtalstraße 6, 8010 Graz, Austria.

Institute of Pharmaceutical Sciences, Department of Pharmacognosy, University of Graz, Beethovenstraße 8, 8010 Graz, Austria.

出版信息

Antioxidants (Basel). 2024 Dec 11;13(12):1511. doi: 10.3390/antiox13121511.

DOI:10.3390/antiox13121511
PMID:39765838
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11673888/
Abstract

High-density lipoproteins (HDL) exist in various subclasses, with smaller HDL particles possessing the highest anti-oxidative and anti-inflammatory properties. Understanding the role of these specific subclasses in chronic kidney disease (CKD) could provide valuable insights into disease progression and potential therapeutic targets. In the present study, we assessed HDL subclass composition in 463 patients with CKD stage 2-4 using nuclear magnetic resonance spectroscopy. Over a mean follow-up period of 5.0 years, 18.6% of patients died. Compared to survivors, deceased patients exhibited significantly lower levels of cholesterol, ApoA-I, and ApoA-II within the small and extra-small (XS) HDL subclasses. Multivariable Cox regression analysis, adjusted for traditional cardiovascular and renal risk factors, demonstrated that reduced levels of XS-HDL-cholesterol, XS-HDL-ApoA-I, and XS-HDL-ApoA-II were independently associated with an increased risk of mortality. Furthermore, receiver operating characteristic analysis identified XS-HDL-ApoA-II as the most potent prognostic marker for mortality. In conclusion, reduced small and XS-HDL subclasses, especially XS-HDL-ApoA-II, are strongly associated with increased all-cause mortality risk in CKD patients. Assessment of HDL subclass distribution could provide valuable clinical information and help identify patients at high risk.

摘要

高密度脂蛋白(HDL)存在多种亚类,较小的HDL颗粒具有最强的抗氧化和抗炎特性。了解这些特定亚类在慢性肾脏病(CKD)中的作用,可为疾病进展及潜在治疗靶点提供有价值的见解。在本研究中,我们使用核磁共振波谱法评估了463例2-4期CKD患者的HDL亚类组成。在平均5.0年的随访期内,18.6%的患者死亡。与存活者相比,死亡患者的小和超小(XS)HDL亚类中的胆固醇、载脂蛋白A-I和载脂蛋白A-II水平显著降低。在对传统心血管和肾脏危险因素进行校正的多变量Cox回归分析中,XS-HDL-胆固醇、XS-HDL-载脂蛋白A-I和XS-HDL-载脂蛋白A-II水平降低与死亡风险增加独立相关。此外,受试者工作特征分析确定XS-HDL-载脂蛋白A-II是最有效的死亡预后标志物。总之,小和XS-HDL亚类减少,尤其是XS-HDL-载脂蛋白A-II,与CKD患者全因死亡风险增加密切相关。评估HDL亚类分布可提供有价值的临床信息,并有助于识别高危患者。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c78/11673888/ad659be7c1f4/antioxidants-13-01511-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c78/11673888/b00b0f73405e/antioxidants-13-01511-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c78/11673888/baff007c9ab7/antioxidants-13-01511-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c78/11673888/ad659be7c1f4/antioxidants-13-01511-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c78/11673888/b00b0f73405e/antioxidants-13-01511-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c78/11673888/baff007c9ab7/antioxidants-13-01511-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c78/11673888/ad659be7c1f4/antioxidants-13-01511-g003.jpg

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本文引用的文献

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BMC Nephrol. 2024 Nov 7;25(1):400. doi: 10.1186/s12882-024-03808-3.
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Chronic Kidney Disease Progression-A Challenge.慢性肾脏病进展——一项挑战
Biomedicines. 2024 Sep 27;12(10):2203. doi: 10.3390/biomedicines12102203.
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Impaired HDL antioxidant and anti-inflammatory functions are linked to increased mortality in acute heart failure patients.载脂蛋白功能障碍与急性心力衰竭患者死亡率增加有关。
Redox Biol. 2024 Oct;76:103341. doi: 10.1016/j.redox.2024.103341. Epub 2024 Sep 5.
4
Low LCAT activity is linked to acute decompensated heart failure and mortality in patients with CKD.低 LCAT 活性与 CKD 患者的急性失代偿性心力衰竭和死亡率相关。
J Lipid Res. 2024 Sep;65(9):100624. doi: 10.1016/j.jlr.2024.100624. Epub 2024 Aug 20.
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HDL-based therapeutics: A promising frontier in combating viral and bacterial infections.基于高密度脂蛋白的治疗方法:抗击病毒和细菌感染的有前途的前沿领域。
Pharmacol Ther. 2024 Aug;260:108684. doi: 10.1016/j.pharmthera.2024.108684. Epub 2024 Jul 2.
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