Lo Cicero Lorenzo, Lentini Paolo, Sessa Concetto, Castellino Niccolò, D'Anca Ambra, Torrisi Irene, Marcantoni Carmelita, Castellino Pietro, Santoro Domenico, Zanoli Luca
School of Nephrology, Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy.
Nephrology and Dialysis, San Bassiano Hospital, Bassano del Grappa, Italy.
Cardiorenal Med. 2025;15(1):29-40. doi: 10.1159/000542965. Epub 2024 Dec 4.
Patients with chronic kidney disease (CKD) have an increased cardiovascular (CV) risk. The lower the glomerular filtration rate, the higher the CV risk.
Current data suggest that several uremic toxins lead to vascular inflammation and oxidative stress that, in turn, lead to endothelial dysfunction, changes in smooth muscle cells' phenotype, and increased degradation of elastin and collagen fibers. These processes lead to both functional and structural arterial stiffening and explain part of the increased risk of acute myocardial infarction and stroke reported in patients with CKD. Considering that, at least in patients with end-stage kidney disease, the reduction of arterial stiffness is associated with a parallel decrease of the CV risk; vascular function is a potential target for therapy to reduce the CV risk.
In this review, we explore mechanisms of vascular dysfunction in CKD, paying particular attention to inflammation, reporting current data in other models of mild and severe inflammation, and discussing the vascular effect of several drugs currently used in nephrology.
慢性肾脏病（CKD）患者心血管（CV）风险增加。肾小球滤过率越低，心血管风险越高。
目前的数据表明，几种尿毒症毒素会导致血管炎症和氧化应激，进而导致内皮功能障碍、平滑肌细胞表型改变以及弹性蛋白和胶原纤维降解增加。这些过程导致功能性和结构性动脉僵硬，并解释了CKD患者急性心肌梗死和中风风险增加的部分原因。考虑到至少在终末期肾病患者中，动脉僵硬的减轻与心血管风险的平行降低相关；血管功能是降低心血管风险治疗的潜在靶点。
在本综述中，我们探讨CKD中血管功能障碍的机制，特别关注炎症，报告其他轻度和重度炎症模型中的当前数据，并讨论目前肾脏病学中使用的几种药物的血管效应。
