Evidence map›Paper›PMID 24339523›Full record

ArticleIndian journal of nephrology2013

Contribution of GSTM1, GSTT1, and MTHFR polymorphisms to end-stage renal disease of unknown etiology in Mexicans.

B E Gutiérrez-Amavizca, R Orozco-Castellanos, R Ortíz-Orozco, J Padilla-Gutiérrez, Y Valle, N Gutiérrez-Gutiérrez, G García-García, M Gallegos-Arreola, L E Figuera

Open access · diamondAbstract read
In one paragraph

Article in Indian journal of nephrology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
0.6field-weighted citation impact, top 32% 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

16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Association of GSTM1 Deletion With Progression of CKD in Children: Findings From the Chronic Kidney Disease in Children (CKiD) Study.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2022
    Observational
  9. Hypertension (Dallas, Tex. : 1979) · 2021
    Review
  10. Absence ofFrontiers in oncology · 2021
    Article
  11. Article
  12. Frontiers in genetics · 2019
    Article
  13. The Loss ofJournal of the American Society of Nephrology : JASN · 2017
    Article
  14. Article
  15. Article
  16. 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

9 authors at 1 institution in 1 country.

B E Gutiérrez-AmavizcaDivision of Genetics, Biomedical Research Center of the West, IMSS, Guadalajara, Jalisco, México ; PhD in Human Genetics, University Center of Health Sciences, University of Guadalajara, Guadalajara, Jalisco, México.
R Orozco-Castellanos
R Ortíz-Orozco
J Padilla-Gutiérrez
Y Valle
N Gutiérrez-Gutiérrez
G García-García
M Gallegos-Arreola
L E Figuera
Universidad de Guadalajara · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress is increased in chronic kidney disease, owing to an imbalance between the oxidative and antioxidant pathways as well as a state of persistent hyperhomocysteinemia. The enzymes glutathione S-transferases (GSTs) and methylenetetrahydrofolate reductase (MTHFR) are implicated in the regulation of these pathways. This study investigates the association between polymorphisms in the Glutathione S-transferase Mu 1 (GSTM1), glutathione S-transferase theta 1 (GSTT1), and MTHFR genes and end-stage renal disease (ESRD) of unknown etiology in patients in Mexico. A Case-control study included 110 ESRD patients and 125 healthy individuals. GSTM1 and GSTT1 genotypes were determined using the multiplex polymerase chain reaction (PCR). The MTHFR C677T polymorphism was studied using a PCR/restriction fragment length polymorphism method. In ESRD patients, GSTM1 and GSTT1 null genotype frequencies were 61% and 7% respectively. GSTM1 genotype frequencies differed significantly between groups, showing that homozygous deletion of the GSTM1 gene was associated with susceptibility to ESRD of unknown etiology (P = 0.007, odds ratios = 2.05, 95% confidence interval 1.21-3.45). The MTHFR C677T polymorphism genotype and allele distributions were similar in both groups (P > 0.05), and the CT genotype was the most common genotype in both groups (45.5% and 46.6%). Our findings suggest that the GSTM1 null polymorphism appears to be associated with the ESRD of unknown etiology in patients in Mexico.

Indexed as

End-stage renal diseaseglutathione S-transferasesmethylenetetrahydrofolate reductasepolymorphism

Identifiers

PMID24339523
PMCPMC3841513
OpenAlexW1984495871

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.