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Claudins in Renal Physiology and Pathology
Caroline Prot-Bertoye1,2,3,4,5, Pascal Houillier1,2,3,4,5
1Centre de Recherche des Cordeliers, INSERM, Sorbonne Université, Université de Paris, F-75006 Paris, France.
Genes
|March 14, 2020
Summary
Claudins are key proteins in kidney tight junctions. Variants in CLDN10b, CLDN16, and CLDN19 cause rare human syndromes affecting kidney function.
Area of Science:
- Nephrology
- Cell Biology
- Genetics
Background:
- Claudins are integral proteins forming tight junctions in epithelial and endothelial cells.
- Specific claudin expression in kidney tubules dictates paracellular pathway permeability and ion selectivity.
- Three claudins (CLDN10b, CLDN16, CLDN19) are linked to rare human kidney syndromes.
Purpose of the Study:
- To review the physiology of mammalian tight junctions and paracellular ion transport.
- To summarize the role of CLDN10b, CLDN16, and CLDN19 in kidney health and disease.
- To discuss CLDN14's potential role due to interactions with CLDN16 and associations with kidney stones.
Main Methods:
- Literature review of claudin physiology and disease associations.
- Analysis of claudin expression patterns, function, and pathogenic variants.
- Examination of single-nucleotide polymorphisms (SNPs) related to urinary calcium and kidney stones.
Main Results:
- CLDN10b variants cause HELIX syndrome.
- CLDN16 or CLDN19 variants cause familial hypomagnesemia with hypercalciuria and nephrocalcinosis.
- CLDN14 SNPs are associated with urinary calcium excretion and kidney stones, suggesting a potential role in renal function.
Conclusions:
- Claudins play critical roles in kidney paracellular transport and are implicated in rare genetic disorders.
- Understanding claudin function is essential for diagnosing and potentially treating kidney diseases.
- Further research into CLDN14's role may offer insights into common kidney stone formation.
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