Zacchia Miriam, Trepiccione Francesco, Morelli Franco, Pani Antonello, Capasso Giovambattista
Department of Internal Medicine, Faculty of Medicine, Second University of Naples, Naples - Italy.
J Nephrol. 2008 Nov-Dec;21(6):836-42.
The nephrotic syndrome is a frequent clinical condition characterized by fluid and salt retention. Although several theories have been put forward to explain the salt-retaining status, recent data have confirmed previous renal micropuncture observations indicating that the distal nephron is the site for increased salt reabsorption, eventually leading to sodium retention. Target proteomic approaches and immunocytochemistry experiments have identified the epithelial sodium channel (ENaC) and basolateral Na+,K+-ATPase as the main transport proteins responsible for increased transepithelial sodium reabsorption in various forms of experimental nephrotic syndrome. Although the fine-tuning for the up-regulation of these transporters has not been so far elucidated, it is clear from clinical studies that the use of amiloride, a selective, dose-dependent ENaC inhibitor, is an appropriate tool to reduce distal sodium reabsorption and thus to offset edema formation.
肾病综合征是一种常见的临床病症，其特征为液体和盐分潴留。尽管已经提出了几种理论来解释盐分潴留状态，但最近的数据证实了先前肾脏微穿刺观察结果，表明远端肾单位是盐分重吸收增加的部位，最终导致钠潴留。靶向蛋白质组学方法和免疫细胞化学实验已确定上皮钠通道（ENaC）和基底外侧钠钾ATP酶是各种形式实验性肾病综合征中跨上皮钠重吸收增加的主要转运蛋白。尽管迄今为止尚未阐明这些转运蛋白上调的精细调节机制，但临床研究清楚地表明，使用氨氯地平（一种选择性、剂量依赖性的ENaC抑制剂）是减少远端钠重吸收从而抵消水肿形成的合适工具。
