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慢性肾脏病中非传统的心血管致病因素:矿物质失衡与尿毒症毒素蓄积

The Non-Traditional Cardiovascular Culprits in Chronic Kidney Disease: Mineral Imbalance and Uremic Toxin Accumulation.

作者信息

Lu Yue, Meng Linlin, Wang Xinlu, Zhang Yun, Zhang Cheng, Zhang Meng

机构信息

State Key Laboratory for Innovation and Transformation of Luobing Theory, Key Laboratory of Cardiovascular Remodeling and Function Research of MOE, NHC, CAMS and Shandong Province, Department of Cardiology, Qilu Hospital of Shandong University, Cheeloo College of Medicine, Shandong University, Jinan 250012, China.

出版信息

Int J Mol Sci. 2025 Aug 17;26(16):7938. doi: 10.3390/ijms26167938.

DOI:10.3390/ijms26167938
PMID:40869261
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12386287/
Abstract

Chronic kidney disease (CKD) is associated with a significantly elevated mortality rate, primarily due to cardiovascular disease (CVD), highlighting a complex bidirectional relationship between the two conditions. Life-threatening cardiovascular events occur despite control of the traditional risk factors, emphasizing the underlying role of non-traditional risk factors. CKD, causing mineral imbalance and the accumulation of uremic toxins due to a compromised ability to excrete waste products, imposes extra pressure on the cardiovascular system. The retention of mineral and uremic toxins, in turn, aggravates the progression of CKD. This review aims to elucidate the pathophysiological connections between CKD and CVD, with a particular focus on the metabolic regulatory mechanisms influenced by minerals such as calcium and phosphate, as well as uremic toxins. We review how these factors contributed to accelerated multi-organ damage through mechanisms such as inflammation, endothelial dysfunction, oxidative stress, and vascular calcification. In addition, we discuss the therapeutic strategies for specific uremic toxins and proposed directions for future investigations. This review provides insights into the complex interplay between metabolic dysregulation and cardiovascular outcomes in CKD patients, promoting the development of innovative therapeutic interventions, ultimately improving the prognosis and quality of life for patients affected by these interconnected conditions.

摘要

慢性肾脏病(CKD)与死亡率显著升高相关,主要原因是心血管疾病(CVD),这凸显了这两种疾病之间复杂的双向关系。尽管传统危险因素得到了控制,但仍会发生危及生命的心血管事件,这强调了非传统危险因素的潜在作用。CKD由于排泄废物的能力受损,导致矿物质失衡和尿毒症毒素蓄积,给心血管系统带来额外压力。而矿物质和尿毒症毒素的潴留反过来又会加重CKD的进展。本综述旨在阐明CKD与CVD之间的病理生理联系,特别关注钙和磷等矿物质以及尿毒症毒素所影响的代谢调节机制。我们回顾了这些因素如何通过炎症、内皮功能障碍、氧化应激和血管钙化等机制导致多器官损害加速。此外,我们还讨论了针对特定尿毒症毒素的治疗策略以及未来研究的方向。本综述深入探讨了CKD患者代谢失调与心血管结局之间的复杂相互作用,推动创新治疗干预措施的发展,最终改善受这些相互关联疾病影响患者的预后和生活质量。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d4c/12386287/54ff09dd18b9/ijms-26-07938-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d4c/12386287/54ff09dd18b9/ijms-26-07938-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d4c/12386287/54ff09dd18b9/ijms-26-07938-g001.jpg

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本文引用的文献

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Eur J Med Res. 2025 Jul 26;30(1):673. doi: 10.1186/s40001-025-02942-4.
2
Klotho Suppresses Indoxyl Sulfate-Mediated Apoptosis in Human Kidney Proximal Tubular (HK-2) Cells through Modulating the AKT/Nrf2 Mechanism.α-klotho通过调节AKT/Nrf2机制抑制硫酸吲哚酚介导的人肾近端小管(HK-2)细胞凋亡。
ACS Omega. 2025 Jun 3;10(23):24018-24029. doi: 10.1021/acsomega.4c08038. eCollection 2025 Jun 17.
3
High-flux hemodialysis with polymethylmethacrylate membranes reduces soluble CD40L, a mediator of cardiovascular disease in uremia.
使用聚甲基丙烯酸甲酯膜进行高通量血液透析可降低可溶性CD40L,其为尿毒症中心血管疾病的一种介质。
Nephrol Dial Transplant. 2025 Jun 6. doi: 10.1093/ndt/gfaf101.
4
Bupropion decreases plasma levels of asymmetric dimethylarginine and ameliorates renal injury by modulation of Ddah1, Oatp4c1, Oct2, and Mate1 in rats with adenine-induced chronic renal injury.安非他酮可降低腺嘌呤诱导的慢性肾损伤大鼠血浆中不对称二甲基精氨酸水平,并通过调节二甲基精氨酸二甲胺水解酶1、有机阴离子转运多肽4C1、有机阳离子转运体2和多药及毒素外排蛋白1来改善肾损伤。
Front Pharmacol. 2025 May 22;16:1565713. doi: 10.3389/fphar.2025.1565713. eCollection 2025.
5
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Am J Physiol Heart Circ Physiol. 2025 Jul 1;329(1):H191-H205. doi: 10.1152/ajpheart.00530.2024. Epub 2025 May 8.
8
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