ReviewPediatric nephrology (Berlin, Germany)2020
Bartter and Gitelman syndromes: Questions of class.
Review in Pediatric nephrology (Berlin, Germany), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Ultra-rare severe kidney dysplasia mimicking salt-wasting tubulopathy associated with TFCP2L1 gene variants.Pediatric nephrology (Berlin, Germany) · 2026Article
- 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
- Identification of Three NovelGenes · 2026Review
- Gitelman and Bartter Syndrome in a Patient With Morbid Obesity: A Case Report and Literature Review.Clinical case reports · 2026Article
- A newborn with type 1 Bartter syndrome: challenges in the treatment and development during 30 months follow-up-a case report.Frontiers in pediatrics · 2026Article
- Gitelman syndrome presenting with lower limb paralysis: a case report.Journal of medical case reports · 2025Article
- Gitelman syndrome in a pediatric patient: a case report and literature review.Frontiers in pediatrics · 2025Article
- Persistent renal dysfunction post-chemotherapy: a diagnostic conundrum in pediatric cancer survivorship - a case report.BMC pediatrics · 2024Article
- Renal Hypokalemia: An Endocrine Perspective.The Journal of clinical endocrinology and metabolism · 2024Review
- Hypokalemia in a young man…think Bartter syndrome type 3.Annals of medicine and surgery (2012) · 2024Article
- Review of childhood genetic nephrolithiasis and nephrocalcinosis.Frontiers in genetics · 2024Review
- Gitelman Syndrome and Hypertension: A Case Report.Cureus · 2023Article
- Genetic diagnosis and treatment of hereditary renal tubular disease with hypokalemia and alkalosis.Journal of nephrology · 2023Review
- Bartter Syndrome: Perspectives of a Pediatric Nephrologist.Electrolyte & blood pressure : E & BP · 2022Review
- Parathyroid hormone and phosphate homeostasis in patients with Bartter and Gitelman syndrome: an international cross-sectional study.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2022Article
- Clinical Course and Prognosis of Tubulopathies Characterized by Metabolic Alkalosis in Children.Turkish archives of pediatrics · 2022Article
- The Bartter-Gitelman Spectrum: 50-Year Follow-up With Revision of Diagnosis After Whole-Genome Sequencing.Journal of the Endocrine Society · 2022Article
- Review
- Renal calcium and magnesium handling in Gitelman syndrome.American journal of translational research · 2022Review
- Twelve exonic variants in theFrontiers in genetics · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bartter and Gitelman syndromes are rare inherited tubulopathies characterized by hypokalaemic, hypochloraemic metabolic alkalosis. They are caused by mutations in at least 7 genes involved in the reabsorption of sodium in the thick ascending limb (TAL) of the loop of Henle and/or the distal convoluted tubule (DCT). Different subtypes can be distinguished and various classifications have been proposed based on clinical symptoms and/or the underlying genetic cause. Yet, the clinical phenotype can show remarkable variability, leading to potential divergences between classifications. These problems mostly relate to uncertainties over the role of the basolateral chloride exit channel CLCNKB, expressed in both TAL and DCT and to what degree the closely related paralogue CLCNKA can compensate for the loss of CLCNKB function. Here, we review what is known about the physiology of the transport proteins involved in these disorders. We also review the various proposed classifications and explain why a gene-based classification constitutes a pragmatic solution.
Indexed as
Identifiers
What OpenQuestion holds
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.