ArticleInternational journal of clinical and experimental pathology2018
Clinical features and genetic findings in Chinese children with distal renal tubular acidosis.
Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Clinical and variant spectrum of patients harboringTranslational pediatrics · 2025Article
- Research progress on renal calculus associate with inborn error of metabolism.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2023Review
- Mutations and clinical characteristics of dRTA caused byFrontiers in pediatrics · 2023Review
- Article
- Genotype-Phenotype Correlation Reanalysis in 83 Chinese Cases withGenetics research · 2022Article
- Next-Generation Sequencing-Based Genetic Diagnostic Strategies of Inherited Kidney Diseases.Kidney diseases (Basel, Switzerland) · 2021Review
- Clinical and Genetic Features in 31 Serial Chinese Children With Gitelman Syndrome.Frontiers in pediatrics · 2021Article
- Claudins in Renal Physiology and Pathology.Genes · 2020Review
- Distal renal tubular acidosis: genetic causes and management.World journal of pediatrics : WJP · 2019Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Distal renal tubular acidosis (dRTA) is characterized by metabolic acidosis due to uric acid dysfunction. The aim of this study was to demonstrate the genetic diagnosis of Chinese children with dRTA by whole-exome sequencing. From Jan. 2010 to Sept. 2015, 16 children with dRTA were recruited to investigate the possibility of genetic diagnosis and to examine any genotype-phenotype relationships in these patients. Sanger sequencing was used to confirm mutations identified by whole-exome sequencing. Clinical and biological features in the patients included hyperchloremic metabolic acidosis, impaired growth, hypokalemia, nephrocalcinosis, nephrolithiasis, hypercalciuria, hypocitraturia, and rickets or osteomalacia. Seventeen mutations in the solute carrier family 4 member 1 (
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Identifiers
31949730PMC6962865W3027449933What 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.