Evidence map›Paper›PMID 31930100›Full record

ArticleAnnals of translational medicine2019

The pathogenic AGT c.856+1G>T mutation of a patient with multiple renal cysts and hypertension.

Wenqing Chen, Bingjue Li, Sha Jia, Qixia Shen, Chong Luo, Yucheng Wang, Shi Feng, Xiujin Shen, Chunhua Weng, Hong Jiang and 1 more

Open access · diamondAbstract readCase Reports
PubMed Full text at PMC Publisher
In one paragraph

Article in Annals of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 46% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Wenqing ChenKidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.
Bingjue LiKidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.
Sha JiaKidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.
Qixia ShenKidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.
Chong LuoKidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.
Yucheng WangKidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.
Shi FengKidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.
Xiujin ShenKidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.
Chunhua WengKidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.
Hong JiangKidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.
Jianghua ChenKidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.
State Administration of Traditional Chinese Medicine of the People's Republic of China · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiotensinogen (AGT) is an essential member of the renin-angiotensin system (RAS); this system regulates blood pressure and affects the physiological function of the kidney. Studies found that mutations of the human AGT gene are involved in diseases such as recessive renal tubular dysgenesis (RTD) and essential hypertension (EHT). Here, we report a 29-year-old male Chinese with essential hypertension and cystic kidney disease. Exome sequencing analysis of the patient and his parents revealed a mutation in the splice donor site of intron 2 of the AGT gene, c.856+1G>T. This mutation was a heterozygous form and inherited from his mother, and the mother was diagnosed with essential hypertension lasting over 20 years. Function prediction of c.856+1G>T mutation using online software showed this intron mutation may affect protein features by destroying the normal splice site. These findings suggest that this intron mutation of the AGT gene is related to the patient's essential hypertension and cystic kidney disease.

Indexed as

AGT genehypertensionintron mutationRenal cyst

Identifiers

PMID31930100
PMCPMC6944549
OpenAlexW2989625635

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.