ArticleClinical kidney journal2014
A severe phenotype of Gitelman syndrome with increased prostaglandin excretion and favorable response to indomethacin.
Article in Clinical kidney journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- The role of SLC12A3 gene variant c.1964G > A in co-existing Gitelman syndrome and unilateral limb paralysis: a case report and literature review.BMC nephrology · 2025Review
- Adult-Onset Gitelman Syndrome: Case Analysis and Literature Review.Case reports in medicine · 2025Article
- Advances in Diagnosis and Treatment of Inherited Kidney Diseases in Children.Kidney diseases (Basel, Switzerland) · 2024Review
- Navigating the multifaceted intricacies of the NaPhysiological reviews · 2024Review
- Long-Term Indomethacin Treatment in a Chinese Child with Gitelman Syndrome: Case Report and Literature Review on its Efficacy and Tolerance.The American journal of case reports · 2023Review
- Genotypic variability in patients with clinical diagnosis of Bartter syndrome type 3.Scientific reports · 2023Article
- The Impact of Gitelman Syndrome on Cardiovascular Disease: From Physiopathology to Clinical Management.Reviews in cardiovascular medicine · 2022Review
- Molecular Basis, Diagnostic Challenges and Therapeutic Approaches of Bartter and Gitelman Syndromes: A Primer for Clinicians.International journal of molecular sciences · 2021Review
- Diagnosis and outpatient management of Gitelman syndrome from the first trimester of pregnancy.BMJ case reports · 2021Article
- Review and Analysis of Two Gitelman Syndrome Pedigrees Complicated with Proteinuria or Hashimoto's Thyroiditis Caused by Compound HeterozygousBioMed research international · 2021Article
- Increased urinary prostaglandin E2 metabolite: A potential therapeutic target of Gitelman syndrome.PloS one · 2017Article
- 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
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our understanding of Gitelman syndrome (GS) and Bartter syndrome has continued to evolve with the use of genetic testing to more precisely define the tubular defects responsible. GS is caused by mutations in the SLC12A3 gene encoding the Na(+)-Cl(-) co-transporter of the distal convoluted tubule (NCCT) and tends to be associated with a milder salt-losing phenotype. We describe two female siblings presenting in infancy with a severe salt-losing tubulopathy and failure to thrive due to compound heterozygous mutations in the SLC12A3 gene encoding the NCCT. Both children were treated with indomethacin resulting in improved linear growth and polyuria. Some atypical biochemical findings in our cases are discussed including raised urinary prostaglandin (PGE2) excretion that normalized with intravenous fluid repletion.
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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.