ArticleTurkish archives of pediatrics2022
Clinical Course and Prognosis of Tubulopathies Characterized by Metabolic Alkalosis in Children.
Article in Turkish archives of pediatrics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 1 citations in OpenAlex.
- Molecular Genetics of Bartter Syndrome: Bridging Genotype-Phenotype Correlations and Precision Therapeutics.Current issues in molecular biology · 2026Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveBartter syndrome and Gitelman syndrome are rare inherited tubulopathies characterized by hypokalemic, hypochloremic metabolic alkalosis. This study aimed to clarify the frequency of the phenotypic and genotypic subgroups, clinical features, long-term management, and prognosis of children diagnosed with Bartter syndrome and Gitelman syndrome in this study. MATERIALS AND
methodsTwenty-seven patients with Bartter syndrome and 6 patients with Gitelman syndrome, who were followed up between 2004 and 2020 in a single center, were included in the study.
resultsThe median age of diagnosis was 4 months in patients with Bartter syndrome and 174 months in patients with Gitelman syndrome. At the last follow-up, a total of 12 Bartter syndrome patients had chronic kidney disease with a mean 7.79 ± 4.73 years of age; 5 (18.5%) of these patients had chronic kidney disease stage 2, 5 (18.5%) had chronic kidney disease stage 3, and 2 (7.4%) had chronic kidney disease stage 5. Of the 5 patients with Bartter syndrome with chronic kidney disease stage 2, 2 had CLCNKB and 1 had SLC12A1 gene mutation. Also, CLCNKB mutation was detected in 2 of 5 patients with Bartter syndrome with chronic kidney disease stage 3. Finally, 2 patients with Bartter syndrome with chronic kidney disease stage 5 had BSND mutation in one and CLCNKB mutation in the other. Estimated glomerular filtration rates of all patients with Gitelman syndrome were normal at the last follow-up. There was no statistically significant association of development of chronic kidney disease with genetic mutation, nephrocalcinosis, prematurity, and hypokalemia.
conclusionPatients with Bartter syndrome and Gitelman syndrome may have a different clinical course due to the underlying genetic mutation. Bartter syndrome and Gitelman syndrome require lifelong treatment, and regular follow-up is important to prevent advanced-stage chronic kidney disease.
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