ArticleJCI insight2021
Impairment in renal medulla development underlies salt wasting in Clc-k2 channel deficiency.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Reduced Expression of Magnesium Transport Proteins in the Distal Convoluted Tubule of Clcnkb-Deficient Mice May Explain Urinary Magnesium Wasting in Classical Bartter Syndrome.Acta physiologica (Oxford, England) · 2026Article
- Whole-organ single-cell mapping defines growth dynamics and clonal organization in developing and adult zebrafish livers.PLoS biology · 2026Article
- Molecular Genetics of Bartter Syndrome: Bridging Genotype-Phenotype Correlations and Precision Therapeutics.Current issues in molecular biology · 2026Review
- An epithelial morphogenetic program for maximal urine concentration.Nature communications · 2026Article
- Mechanism of Gating and Isoform-Specific Inhibition in Renal CLC Chloride Channels.bioRxiv : the preprint server for biology · 2026Article
- Article
- Intercalated Cell ClC-K2 Channel Contributes to Systemic ClFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Rapid lightsheet fluorescence imaging of whole Drosophila brains at nanoscale resolution by potassium acrylate-based expansion microscopy.Nature communications · 2024Article
- Subdiffraction Imaging of Cleared and Expanded Large-Scale Tissues.Chemical & biomedical imaging · 2024Review
- Transport activity regulates mitochondrial bioenergetics and biogenesis in renal tubules.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Review
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 3 countries.
Funding
Abstract
The prevailing view is that the ClC-Ka chloride channel (mouse Clc-k1) functions in the thin ascending limb to control urine concentration, whereas the ClC-Kb channel (mouse Clc-k2) functions in the thick ascending limb (TAL) to control salt reabsorption. Mutations of ClC-Kb cause classic Bartter syndrome, characterized by renal salt wasting, with perinatal to adolescent onset. We studied the roles of Clc-k channels in perinatal mouse kidneys using constitutive or inducible kidney-specific gene ablation and 2D and advanced 3D imaging of optically cleared kidneys. We show that Clc-k1 and Clc-k2 were broadly expressed and colocalized in perinatal kidneys. Deletion of Clc-k1 and Clc-k2 revealed that both participated in NKCC2- and NCC-mediated NaCl reabsorption in neonatal kidneys. Embryonic deletion of Clc-k2 caused tubular injury and impaired renal medulla and TAL development. Inducible deletion of Clc-k2 beginning after medulla maturation produced mild salt wasting resulting from reduced NCC activity. Thus, both Clc-k1 and Clc-k2 contributed to salt reabsorption in TAL and distal convoluted tubule (DCT) in neonates, potentially explaining the less-severe phenotypes in classic Bartter syndrome. As opposed to the current understanding that salt wasting in adult patients with Bartter syndrome is due to Clc-k2 deficiency in adult TAL, our results suggest that it originates mainly from defects occurring in the medulla and TAL during development.
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Registered trials
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