蛋白酵素
肾病综合征
上皮钠通道
激肽释放酶
丝氨酸
钠
化学
丝氨酸蛋白酶
尿潴留
抑肽酶
医学
内科学
蛋白酶
内分泌学
药理学
生物化学
酶
泌尿科
有机化学
作者
Ferruh Artunç,Matthias Wörn,Anja Schork,Bernhard N. Bohnert
摘要
Abstract Sodium retention and extracellular volume expansion are typical features of patients with nephrotic syndrome. In recent years, from in vitro data, endoluminal activation of the epithelial sodium channel (ENaC) by aberrantly filtered serine proteases has been proposed as an underlying mechanism. Recently, this concept was supported in vivo in nephrotic mice that were protected from proteolytic ENaC activation and sodium retention by the use of aprotinin for the pharmacological inhibition of urinary serine protease activity. These and other findings from studies in both rodents and humans highlight the impact of active proteases in the urine, or proteasuria, on ENaC‐mediated sodium retention and edema formation in nephrotic syndrome. Targeting proteasuria could become a therapeutic approach to treat patients with nephrotic syndrome. However, pathophysiologically relevant proteases remain to be identified. In this review, we introduce the concept of proteasuria to explain tubular sodium avidity and conclude that proteasuria can be considered as a key mechanism of sodium retention in patients with nephrotic syndrome.
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