ReviewAmerican journal of translational research2022
Renal calcium and magnesium handling in Gitelman syndrome.
Review in American journal of translational research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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.
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
10 citing papers in PubMed, 8 citations in OpenAlex.
- Article
- Clinical and genetic features of Gitelman syndrome patients with hyperuricemia.Clinical kidney journal · 2025Article
- Article
- 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
- Pathophysiological role of Na-Cl cotransporter in kidneys, blood pressure, and metabolism.Human cell · 2024Review
- Navigating the multifaceted intricacies of the NaPhysiological reviews · 2024Review
- Renal Hypokalemia: An Endocrine Perspective.The Journal of clinical endocrinology and metabolism · 2024Review
- Novel compound heterozygous variants ofFrontiers in genetics · 2023Article
- Late diagnosis of Gitelman syndrome in an elderly patient: identification of a novel SLC12A3 pathogenic variant.Jornal brasileiro de nefrologiaArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gitelman syndrome (GS) is an autosomal recessive salt-losing tubulopathy caused by biallelic inactivating mutations in the SLC12A3 gene. This gene encodes the thiazide-sensitive sodium-chloride cotransporter (NCC) which is exclusively expressed in the distal convoluted tubules (DCT). GS patients classically present with hypokalemic metabolic alkalosis with hypocalciuria and hypomagnesemia. While hypokalemia and metabolic alkalosis are easily explained by effects of the genotypic defect in GS, the mechanisms by which hypomagnesemia and hypocalciuria develop in GS are poorly understood. In this review, we aim to achieve three major objectives. First, present a concise discussion about current understanding on physiologic calcium and magnesium handling in the DCT. Second, integrate expression data from studies on calciotropic and magnesiotropic proteins relevant to the GS disease state. Lastly, provide insights into the possible mechanisms of calcium-magnesium crosstalk relating to the co-occurrence of hypocalciuria and hypomagnesemia in GS models. Our analyses highlight specific areas of study that are valuable in elucidating possible molecular pathways of hypocalciuria and hypomagnesemia in GS.
Indexed as
Identifiers
35173827PMC8829599W4226227278What 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.