Evidence map›Paper›PMID 29927456›Full record

ReviewJornal brasileiro de nefrologia

NOS3 Polymorphisms and Chronic Kidney Disease.

Alejandro Marín Medina, Eduardo Esteban Zubero, Moisés Alejandro Alatorre Jiménez, Sara Anabel Alonso Barragan, Carlos Arturo López García, José Juan Gómez Ramos, Juan Francisco Santoscoy Gutierrez, Zurisadai González Castillo

Open access · diamondAbstract readReview
In one paragraph

Review in Jornal brasileiro de nefrologia. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 35% 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, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Study of the Active Components and Molecular Mechanism ofFrontiers in molecular biosciences · 2021
    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 5 institutions in 3 countries.

Alejandro Marín MedinaUniversidad de Guadalajara, Centro Universitario de Ciencias de la Salud, Departamento de Genética, Guadalajara, México.
Eduardo Esteban ZuberoUniversidad de Zaragoza, Departamento de Farmacología y Fisiología, Zaragoza, España.
Moisés Alejandro Alatorre JiménezAsociación Mexicana de Atrofia Muscular Espinal, Guadalajara, México.
Sara Anabel Alonso BarraganAsociación Mexicana de Atrofia Muscular Espinal, Guadalajara, México.
Carlos Arturo López GarcíaUniversity of Texas Health Science Center at San Antonio, Department of Cellular and Structural Biology, San Antonio, United States.
José Juan Gómez RamosInstituto Mexicano del Seguro Social (IMSS), Hospital General Regional No. 89, Guadalajara, México.
Juan Francisco Santoscoy GutierrezInstituto Mexicano del Seguro Social, Centro de Investigación Biomedica de Occidente, Departamento de Neurociencia, Guadalajara, México.
Zurisadai González CastilloAsociación Mexicana de Atrofa Muscular Espinal (AMAME), Guadalajara, México.
Asociación Mexicana de Psicología y Desarrollo Comunitario · MXMexican Social Security Institute · MXThe University of Texas at Austin · USUniversidad de Guadalajara · MXUniversidad de Zaragoza · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease (CKD) is a multifactorial pathophysiologic irreversible process that often leads to a terminal state in which the patient requires renal replacement therapy. Most cases of CKD are due to chronic-degenerative diseases and endothelial dysfunction is one of the factors that contribute to its pathophysiology. One of the most important mechanisms for proper functioning of the endothelium is the regulation of the synthesis of nitric oxide. This compound is synthesized by the enzyme nitric oxide synthase, which has 3 isoforms. Polymorphisms in the NOS3 gene have been implicated as factors that alter the homeostasis of this mechanism. The Glu298Asp polymorphisms 4 b/a and -786T>C of the NOS3 gene have been associated with a more rapid deterioration of kidney function in patients with CKD. These polymorphisms have been evaluated in patients with CKD of determined and undetermined etiology and related to a more rapid deterioration of kidney function.

Indexed as

Polymorphism, GeneticHumansNitric Oxide Synthase Type IIIRenal Insufficiency, ChronicNitric Oxide Synthase Type III

Identifiers

PMID29927456
PMCPMC6533959
OpenAlexW2807285359

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.