Claudins and nephrolithiasis

Current Opinion in Nephrology and Hypertension
Allein Plain, R Todd Alexander

Abstract

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. 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. Alterations to claudins expressed in the TAL tight junction greatly affects calcium homeostasis as highlighted by point mutations in claudin-16 ...Continue Reading

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Citations

Oct 5, 2019·International Journal of Molecular Sciences·Enrique Gamero-EstevezAimee K Ryan
Sep 21, 2018·Clinical Journal of the American Society of Nephrology : CJASN·Ronak Jagdeep Shah, John C Lieske
Jan 14, 2021·American Journal of Physiology. Cell Physiology·Shaista AnwerKatalin Szászi
Apr 3, 2021·Pediatric Nephrology : Journal of the International Pediatric Nephrology Association·Mallory L Downie, R Todd Alexander
May 23, 2020·Biochimica Et Biophysica Acta. Biomembranes·Luca Meoli, Dorothee Günzel

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