克洛丹
并行传输
高钙尿症
肾钙质沉着症
紧密连接
肾单位
亨利环
钙
化学
细胞生物学
内分泌学
内科学
肾
生物
磁导率
医学
生物化学
膜
作者
Allein Plain,R. Todd Alexander
出处
期刊:Current Opinion in Nephrology and Hypertension
[Ovid Technologies (Wolters Kluwer)]
日期:2018-07-01
卷期号:27 (4): 268-276
被引量:18
标识
DOI:10.1097/mnh.0000000000000426
摘要
Purpose of review The greatest risk factor for kidney stone formation is increased urinary calcium excretion. Most filtered calcium is reabsorbed from the proximal tubule and the thick ascending limb (TAL) of Henle's loop via a paracellular pathway. Claudins are tight junction proteins that confer the permeability properties of an epithelium. We review the contribution of renal claudins to nephron calcium permeability and how perturbations in these pathways cause alterations in tubular calcium transport, hypercalciuria, nephrocalcinosis, or nephrolithiasis. Recent findings Claudin-16 and Claudin-19 form a complex with claudin-3 enabling divalent cation permeability in the TAL. Claudin-14 interacts with claudin-16 to attenuate calcium permeability through this pore. Intronic mutations in claudin-14 increase expression causing hypercalciuria and kidney stones. A different type of TAL tight junction pore is composed of claudin-10b, which does not preferentially permeate calcium. Deletion of claudin-10b results in increased expression of the claudin-16/claudin-19 complex expressed in the medullary TAL and nephrocalcinosis. Summary Alterations to claudins expressed in the TAL tight junction greatly affects calcium homeostasis as highlighted by point mutations in claudin-16 or claudin-19 causing FHHNC or gain of function mutations in claudin-14 causing kidney stones.
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