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Review
. 2013 Feb;14(1):5-12.
doi: 10.1007/s11934-012-0289-2.

The role of claudin in hypercalciuric nephrolithiasis

Affiliations
Review

The role of claudin in hypercalciuric nephrolithiasis

Jianghui Hou. Curr Urol Rep. 2013 Feb.

Abstract

Calcium nephrolithiasis is a common condition. Family-based genetic linkage studies and genome-wide association studies (GWASs) have uncovered a run of important candidate genes involved in renal Ca(++) disorders and kidney stone diseases. The susceptible genes include NKCC2, ROMK and ClCkb/Barttin that underlie renal salt excretion; claudin-14, -16 and -19 that underlie renal Ca(++) excretion; and CaSR that provides a sensing mechanism for the kidney to regulate salt, water and Ca(++) homeostasis. Biological and physiological analyses have revealed the cellular mechanism for transepithelial Ca(++) transport in the kidney that depends on the concerted action of these gene products. Although the individual pathogenic weight of the susceptible genes in nephrolithiasis remains unclear, perturbation of their expression or function compromises the different steps within the integrated pathway for Ca(++) reabsorption, providing a physiological basis for diagnosing and managing kidney stone diseases.

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Conflict of interest statement

Disclosure The author reported no potential conflicts of interest relevant to this article.

Figures

Fig. 1
Fig. 1
Transepithelial ionic transport in the thick ascending limb of Henle’s loop (TALH). a When similar salt concentrations are present at the luminal and basolateral sides, the luminal spontaneous potential Vte of +8 mV is generated by the concerted action of luminal K+ channels, basolateral Clchannels, the Na+2ClK+ cotransporter, and the Na+, K+-ATPase. Vte drives Na+ absorption through the paracellular pathway. b When a dilute luminal fluid is present after NaCl absorption along the water-impermeable TAL, the luminal potential Vte of +30 mV is now generated as a diffusion voltage by the ‘backleak’ of Na+. The diffusion voltage depends on the cation permselectivity of the tight junction. The membrane voltage (Vm) trace depicts the virtual measurement by an electrode that is pushed from the basolateral side through the cell to the luminal side. Modified from Figure 1 in ref

References

    1. Coe FL, Evan A, Worcester E. Kidney stone disease. J Clin Invest. 2005;115:2598–608. - PMC - PubMed
    1. Hess B, Hasler-Strub U, Ackermann D, et al. Metabolic evaluation of patients with recurrent idiopathic calcium nephrolithiasis. Nephrol Dial Transplant. 1997;12:1362–8. - PubMed
    1. Thorleifsson G, Holm H, Edvardsson V, et al. Sequence variants in the CLDN14 gene associate with kidney stones and bone mineral density. Nat Genet. 2009;41:926–30. - PubMed
    1. Friedman PA. Renal calcium metabolism. Seldin and Giebisch’s The Kidney – Physiology and Pathophysiology. 2008;2(chapter 65):1851–1890.
    1. Mensenkamp AR, Hoenderop JG, Bindels RJ. Recent advances in renal tubular calcium reabsorption. Curr Opin Nephrol Hypertens. 2006;15:524–9. - PubMed

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