Renal Handling of Uric Acid
Renal Handling of Uric Acid
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DOI：
10.1159/000484271
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发表时间：
2018-01-01
期刊：
影响因子：
--
通讯作者：
Flores Fonseca, Milagros M.
中科院分区：
文献类型：
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作者：
Andrade Sierra, Jorge;Flores Fonseca, Milagros M.
高尿酸血症发生在21.4%的成年人群中，与几种增加氧化应激的疾病相关，并有助于疾病发展和进展的炎症机制的发病机制。血清血液或尿液样本的尿酸水平主要用于识别临床问题，这取决于尿酸途径的改变，包括合成，重吸收或排泄。几种特别作为转运蛋白的蛋白质（URAT 1、GLUT 9、1-NPT 1、1-NPT 4、OAT 4、9-MCT 9、hUAT 1等）在最近的过去已经确定涉及导致临床益处的肾小管转运和清除。到目前为止，尿酸稳态的知识集中在了解分子和遗传机制，包括遗传多态性，诱导遗传和获得性肾小管疾病，增加或减少尿酸排泄的主要研究。(c)2018年S. Karger AG，巴塞尔
Hyperuricemia occurs in 21.4% of the adult population and is associated with several conditions that increase oxidative stress and contributes to the pathogenesis of inflammatory mechanisms for the development and progression of diseases. Serum blood or urine samples of uric acid levels were used to mainly identify clinical problems, depending on the uric acid pathway alterations, which include synthesis, reabsorption or its excretion. Several proteins that act particularly as transporters (URAT1, GLUT9, 1-NPT1, 1-NPT4, OAT4, 9-MCT9, hUAT1, etc.) have been identified in the recent past involving tubular transport and clearance leading to clinical benefits. Until now, the knowledge of uric acid homeostasis centers its primary investigation on understanding molecular and genetic mechanisms, including the genetic polymorphisms that induce genetic and acquire renal tubular disorder, which increases or diminishes urate excretion. (c) 2018 S. Karger AG, Basel