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无症状高尿酸血症在慢性肾脏病和心血管疾病进展中的作用。

Role of asymptomatic hyperuricemia in the progression of chronic kidney disease and cardiovascular disease.

作者信息

Waheed Yousuf, Yang Fan, Sun Dong

机构信息

Department of Nephrology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.

Department of Internal Medicine and Diagnostics, Xuzhou Medical University, Xuzhou, China.

出版信息

Korean J Intern Med. 2021 Nov;36(6):1281-1293. doi: 10.3904/kjim.2020.340. Epub 2021 Jul 8.

Abstract

Previous research has investigated whether hyperuricemia serves as an independent risk factor for cardiovascular and renal diseases. Hyperuricemia is defined as an abnormally high level of uric acid (UA; i.e., serum urate level > 6.8 mg/dL). Hyperuricemia has been considered a complication of chronic kidney disease (CKD). However, it seems to play a pathogenic role in the progression of renal diseases. There has been increasing focus on the link between hyperuricemia and CKD. The results of randomized controlled trials have implied independent associations between hyperuricemia and the progression of cardiovascular and renal morbidities. These associations may be mediated by renin-angiotensin system activation, nitric oxide synthase inhibition, and macrovascular/microvascular disease development. There remains controversy regarding the use of serum UA level as an indirect index of renal vascular disease. This literature review focuses on the role of asymptomatic hyperuricemia in the progression of CKD, as well as the association between hyperuricemia and cardiovascular disease. It also provides a general overview of the physiological metabolism of UA.

摘要

先前的研究调查了高尿酸血症是否为心血管疾病和肾脏疾病的独立危险因素。高尿酸血症定义为尿酸(UA;即血清尿酸水平>6.8mg/dL)异常升高。高尿酸血症一直被认为是慢性肾脏病(CKD)的一种并发症。然而,它似乎在肾脏疾病进展中起致病作用。高尿酸血症与CKD之间的联系已受到越来越多的关注。随机对照试验的结果表明高尿酸血症与心血管和肾脏疾病进展之间存在独立关联。这些关联可能由肾素-血管紧张素系统激活、一氧化氮合酶抑制以及大血管/微血管疾病发展介导。关于将血清UA水平用作肾血管疾病的间接指标仍存在争议。这篇文献综述聚焦于无症状高尿酸血症在CKD进展中的作用,以及高尿酸血症与心血管疾病之间的关联。它还概述了UA的生理代谢。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef9b/8588983/cff8a32f720a/kjim-2020-340f1.jpg

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