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Claudins and nephrolithiasis.

Allein Plain¹, R Todd Alexander^1,2,3

¹Departments of Physiology and.

Current Opinion in Nephrology and Hypertension

|May 22, 2018

Summary

This summary is machine-generated.

Renal claudins regulate calcium reabsorption in the kidney. Dysfunctional claudins, particularly claudin-14, claudin-16, and claudin-19, disrupt calcium transport, leading to hypercalciuria and kidney stones.

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Published on: May 26, 2021

Area of Science:

Nephrology
Molecular Biology
Cell Biology

Background:

Kidney stone formation is primarily linked to increased urinary calcium excretion.
Calcium reabsorption in the kidney occurs mainly through paracellular pathways in the proximal tubule and thick ascending limb (TAL).
Claudins, as key tight junction proteins, dictate epithelial permeability, including for divalent cations like calcium.

Purpose of the Study:

To review the role of renal claudins in nephron calcium permeability.
To elucidate how claudin pathway alterations contribute to hypercalciuria, nephrocalcinosis, and nephrolithiasis.

Main Methods:

Review of existing literature on claudin function in renal calcium transport.
Analysis of genetic mutations affecting claudin expression and function.
Examination of the impact of claudin complexes on paracellular calcium flux.

Main Results:

Claudin-16 and Claudin-19 form a complex crucial for calcium permeability in the TAL.
Claudin-14 modulates this complex, with mutations leading to hypercalciuria and kidney stones.
Claudin-10b forms a distinct pore, and its absence increases calcium-permeable claudin complexes, causing nephrocalcinosis.

Conclusions:

Alterations in TAL claudins significantly impact calcium homeostasis.
Mutations in claudin-16 or claudin-19 cause familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC).
Gain-of-function mutations in claudin-14 are a direct cause of kidney stones due to excessive hypercalciuria.