ArticleJournal of the American Society of Nephrology : JASN2011
alphaENaC-mediated lithium absorption promotes nephrogenic diabetes insipidus.
Article in Journal of the American Society of Nephrology : JASN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.
- Molecular mechanisms in lithium-associated renal disease: a systematic review.International urology and nephrology · 2016Pooled it
- Lithium in Bipolar Disorder: Renal Mechanisms, Nephrotoxicity Phenotypes, and a Shared-Care Pathway for Clinical Practice.International journal of molecular sciences · 2026Review
- Lithium effects on renal functioning: an expert opinion and management algorithm.International journal of bipolar disorders · 2026Article
- Lithium nephrotoxicity: a systematic review and meta-analysis of lithium versus non-lithium control studies in patients with affective disorders.Therapeutic advances in psychopharmacology · 2026Review
- Lithium-induced kidney injury and fibrosis: A versatile model to explore cellular pathways of injury and repair.Physiological reports · 2025Review
- Lack of renal NHE1 exacerbates lithium-induced nephrogenic diabetes insipidus.Acta physiologica (Oxford, England) · 2025Article
- A Pedigree Study of Hereditary Diabetes Insipidus Caused by X Chromosome AVPR2 Gene Mutation.International medical case reports journal · 2025Article
- Lithium poisoning and renal replacement therapy: pathophysiology and current clinical recommendations.International urology and nephrology · 2023Review
- Absence of E-Cadherin and β-Catenin in the Basal Plasma Membrane of Collecting Duct Cells During NDI Development and Recovery.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2023Article
- The use of Tablo continuous veno-venous haemodialysis to rapidly remove lithium in a patient with severe lithium toxicity.BMJ case reports · 2023Article
- Early Postnatal Outcome and Care after in Utero Exposure to Lithium: A Single Center Analysis of a Belgian Tertiary University Hospital.International journal of environmental research and public health · 2022Article
- Atorvastatin does not ameliorate nephrogenic diabetes insipidus induced by lithium or potassium depletion in mice.Physiological reports · 2021Article
- SIRT7 modulates the stability and activity of the renal K-Cl cotransporter KCC4 through deacetylation.EMBO reports · 2021Article
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- Targeting the Trafficking of Kidney Water Channels for Therapeutic Benefit.Annual review of pharmacology and toxicology · 2020Review
- Identification ofJournal of the American Society of Nephrology : JASN · 2019Article
- The serine-threonine kinase PIM3 is an aldosterone-regulated protein in the distal nephron.Physiological reports · 2019Article
- Contribution of NHE3 and dietary phosphate to lithium pharmacokinetics.European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences · 2019Article
- Lithium increases ammonium excretion leading to altered urinary acid-base buffer composition.Journal of nephrology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lithium-induced nephrogenic diabetes insipidus (NDI) is accompanied by polyuria, downregulation of aquaporin 2 (AQP2), and cellular remodeling of the collecting duct (CD). The amiloride-sensitive epithelial sodium channel (ENaC) is a likely candidate for lithium entry. Here, we subjected transgenic mice lacking αENaC specifically in the CD (knockout [KO] mice) and littermate controls to chronic lithium treatment. In contrast to control mice, KO mice did not markedly increase their water intake. Furthermore, KO mice did not demonstrate the polyuria and reduction in urine osmolality induced by lithium treatment in the control mice. Lithium treatment reduced AQP2 protein levels in the cortex/outer medulla and inner medulla (IM) of control mice but only partially reduced AQP2 levels in the IM of KO mice. Furthermore, lithium induced expression of H(+)-ATPase in the IM of control mice but not KO mice. In conclusion, the absence of functional ENaC in the CD protects mice from lithium-induced NDI. These data support the hypothesis that ENaC-mediated lithium entry into the CD principal cells contributes to the pathogenesis of lithium-induced NDI.
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Registered trials
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