ArticleInternational journal of nephrology2011
Primary molecular disorders and secondary biological adaptations in bartter syndrome.
Article in International journal of nephrology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- A dual-organ genetic interplay between sensorineural hearing loss and kidney disease: an update for clinicians.Pediatric nephrology (Berlin, Germany) · 2026Review
- An Atypical Presentation of Bartter Syndrome Type 3 With Hypocalciuria and Opisthotonus Posture in a Preterm Infant.Clinical case reports · 2025Article
- A Case of a Novel MAGED2 Mutation Resulting in Non-transient Bartter's Syndrome in an Adult Female.Cureus · 2023Article
- A highly unusual case of osmotic demyelination syndrome and extrapontine myelinolysis in a 3-month-old infant with Bartter syndrome.The Journal of international medical research · 2020Article
- Bartter syndrome: causes, diagnosis, and treatment.International journal of nephrology and renovascular disease · 2018Review
- Unusual Complication of Multidrug Resistant Tuberculosis.Case reports in nephrology · 2017Article
- Increased urinary prostaglandin E2 metabolite: A potential therapeutic target of Gitelman syndrome.PloS one · 2017Article
- Fetal urine biochemistry in antenatal Bartter syndrome: a case report.Clinical case reports · 2016Article
- Management of a severe case of Gitelman syndrome with poor response to standard treatment.BMJ case reports · 2016Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bartter syndrome is a hereditary disorder that has been characterized by the association of hypokalemia, alkalosis, and the hypertrophy of the juxtaglomerular complex with secondary hyperaldosteronism and normal blood pressure. By contrast, the genetic causes of Bartter syndrome primarily affect molecular structures directly involved in the sodium reabsorption at the level of the Henle loop. The ensuing urinary sodium wasting and chronic sodium depletion are responsible for the contraction of the extracellular volume, the activation of the renin-aldosterone axis, the secretion of prostaglandins, and the biological adaptations of downstream tubular segments, meaning the distal convoluted tubule and the collecting duct. These secondary biological adaptations lead to hypokalemia and alkalosis, illustrating a close integration of the solutes regulation in the tubular structures.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.