Evidence map›Paper›PMID 31949506›Full record

ArticleOpen access Macedonian journal of medical sciences2019

Analysis of

Moushira Zaki, Shreen El-Shaer, Sahar Rady, Manal Abd El-Salam, Ragaa Abd-El-Salam, Ibrahim Abdelfattah Alkashlan, Mohamed Saber, Sanaa Mohamed, Mohamed Hassaan, Eman Rabie and 1 more

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

Article in Open access Macedonian journal of medical sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Association BetweenFrontiers in medicine · 2022
    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 4 institutions in 2 countries.

Moushira ZakiBiological Anthropology Department, Medical Research Division, National Research Centre, Cairo, Egypt.
Shreen El-ShaerBiochemistry- Faculty of Pharmacy (Girls), Al-Azhar University, Cairo, Egypt.
Sahar RadyBiochemistry- Faculty of Pharmacy (Girls), Al-Azhar University, Cairo, Egypt.
Manal Abd El-SalamDepartment of Pediatrics (Nephrology Unit), Faculty of Medicine (for Girls), Al-Azhar University, Cairo, Egypt.
Ragaa Abd-El-SalamDepartment of Pediatrics (Nephrology Unit), Faculty of Medicine (for Girls), Al-Azhar University, Cairo, Egypt.
Ibrahim Abdelfattah AlkashlanPediatric Nephrology Unite, Al-Hussein University Hospital, Cairo, Egypt.
Mohamed SaberPediatric Nephrology Unite, Al-Hussein University Hospital, Cairo, Egypt.
Sanaa MohamedBiological Anthropology Department, Medical Research Division, National Research Centre, Cairo, Egypt.
Mohamed HassaanSlagelse Hospital, Internal Medicine Department, Slagelse, Denmark.
Eman RabieMedical Molecular Genetics, National Research Center, Cairo, Egypt.
Khalda AmrMedical Molecular Genetics, National Research Center, Cairo, Egypt.
National Research Centre · EGAl-Azhar University · EGNational Water Research Center · EGSlagelse Hospital · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMutations in the

aimThis study aims to determine the mutation of

methodsThe study included 53 children with NS, and 53 healthy volunteers matched in age and sex controls. The median age at disease onset was 7.3 years. Among NS cases, 31 cases had steroid-sensitive nephrotic syndrome (SSNS) and 22 children with steroid-resistant nephrotic syndrome (SRNS). Polymerase chain reaction amplification of the whole coding region of

resultsNS patients showed a significant higher frequency of heterozygous genotype GA (89.5%) compared to control group (10.5%) with increased risk of NS (OR, 12.04; 95% CI, 2.61 to55.38; p < 0.0001). Moreover, SRNS showed a significant higher frequency of GA genotype (68.2%) than the SSNS group (6.5%). The GA genotype was associated with increased risk of SRNS (OR, 31.1; 95% CI, 5.73 to 168.48; P < 0.001) and the A allele was associated with increased risk of SRNS (OR, 15.52; 95% CI, 3.325 to 72.422; P < .001).

conclusionR229Q polymorphisms are associated with SRNS, and any child with SRNS should be searched for mutations in the

Indexed as

NPHS2 mutationR229Q polymorphismSteroid resistant nephrotic syndrome

Identifiers

PMID31949506
PMCPMC6953933
OpenAlexW2996586575

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.