ArticleKidney international reports2020
Autosomal Recessive Renal Tubular Dysgenesis Caused by a Founder Mutation of Angiotensinogen.
Article in Kidney international reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 22 citations in OpenAlex.
- Non-dialyzable uremic toxins and renal tubular cell damage in CKD patients: a systems biology approach.European journal of medical research · 2024Article
- A loss-of-function AGTR1 variant in a critically-ill infant with renal tubular dysgenesis: case presentation and literature review.BMC nephrology · 2024Review
- Clinical utility of chromosomal microarray analysis and whole exome sequencing in foetuses with oligohydramnios.Annals of medicine · 2023Article
- Analysis of clinically relevant variants from ancestrally diverse Asian genomes.Nature communications · 2022Article
- Effect of Hydrocortisone on Angiotensinogen (Cells · 2021Article
- Editorial: Emerging New Tests and Their Impact Upon the Practice of Reproductive Genetics.Frontiers in genetics · 2021Article
- Rapid Trio Exome Sequencing for Autosomal Recessive Renal Tubular Dysgenesis in Recurrent Oligohydramnios.Frontiers in genetics · 2021Article
- Late Preterm Infant With Postnatal Diagnosis of Renal Tubular Dysgenesis.Journal of investigative medicine high impact case reportsArticle
Corrections and comments
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Authors and funding
16 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionAutosomal recessive renal tubular dysgenesis (ARRTD) caused by inactivation mutations in
methodsWe report 6 Taiwanese individuals with ARRTD from 6 unrelated families diagnosed by renal histology. Clinical features, outcome, and prevalence of carrier heterozygosity were examined.
resultsAll patients exhibited antenatal oligohydramnios, postnatal anuria, pulmonary hypoplasia, and profound hypotension refractory to interventions. Angiotensinogen (AGT) protein levels were diminished in the liver, along with reduced serum AGT, angiotensin I (Ang I) and angiotensin II (Ang II) levels. Neonatal demise occurred in all but 1 case. All individuals carried the same homozygous E3_E4 del:2870bp deletion+9bp insertion in
conclusionThis
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Registered trials
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