Evidence map›Paper›PMID 16521052›Full record

ArticleClinical rheumatology2006

Renin-angiotensin system gene polymorphisms: association with susceptibility to Henoch-Schonlein purpura and renal involvement.

Ozan Ozkaya, Oğuz Söylemezoğlu, Sevim Gönen, Müge Misirlioğlu, Serdar Tuncer, Süleyman Kalman, Necla Buyan, Enver Hasanoğlu

Abstract read
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In one paragraph

Article in Clinical rheumatology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 5 pooled it
1.6field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 5 syntheses or guidelines pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Angiotensin II type 1 receptor polymorphisms and susceptibility to hypertension: a HuGE review.Genetics in medicine : official journal of the American College of Medical Genetics · 2008
    Pooled it
  5. Pooled it
  6. Article
  7. Review
  8. IgA vasculitis or Henoch-Schönlein purpura: genetics and beyond.Pediatric nephrology (Berlin, Germany) · 2021
    Article
  9. Article
  10. Review
  11. 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

8 authors at 1 institution in 1 country.

Ozan OzkayaDepartment of Pediatric Nephrology, Faculty of Medicine, Gazi University, Ankara, Turkey. ozanozkaya@yahoo.com
Oğuz Söylemezoğlu
Sevim Gönen
Müge Misirlioğlu
Serdar Tuncer
Süleyman Kalman
Necla Buyan
Enver Hasanoğlu
Gazi University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The clinical course of Henoch-Schönlein Purpura (HSP) in children is variable, with some patients having a much more rapidly progressing course than others. We investigated whether polymorphisms of the renin-angiotensin system (RAS) genes are involved in HSP. Three RAS genotypes were examined in 114 children with HSP and in 164 healthy children: the angiotensin I converting enzyme (ACE) insertion/deletion polymorphism, the M235T mutation in the angiotensinogen gene (Agt), and the A1166C in the angiotensin II type I receptor (AT1R) gene. Significant differences were observed between HSP patients and control group in the frequency of ACE and Agt genotypes (p=0.004 and p=0.003, respectively). The TT genotype of Agt gene was associated with a 3.5-fold increased risk for Henoch-Schönlein nephritis (HSN) compared with the MM/MT genotype (odds ratio, 3.5; 95% confidence interval, 1.2-10.4). There was a trend to a higher prevalence of the TT genotype of the Agt gene among patients with nephrotic range proteinuria when compared to the patients with mild proteinuria, although the difference did not reach a statistical significance. The results of this study suggest that polymorphisms of ACE gene and Agt gene likely influence the risk of developing HSP. However, among the three genes of the RAS studies, only Agt gene was associated with the susceptibility to HSN. RAS gene polymorphisms studied are not associated with the presence of nephrotic range proteinuria. Additional studies are warranted to verify the correlation between RAS gene polymorphisms and susceptibility to HSP.

Indexed as

Genetic Predisposition to DiseasePolymorphism, GeneticAdolescentAlanineAngiotensinogenChildChild, PreschoolCysteineDNA Transposable ElementsFemaleGene DeletionGene FrequencyGenotypeHumansIgA VasculitisKidney DiseasesAlanineAngiotensinogenCysteineDNA Transposable ElementsMethioninePeptidyl-Dipeptidase AReceptor, Angiotensin, Type 1Threonine

Identifiers

PMID16521052
OpenAlexW2083577644

What OpenQuestion holds

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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.