Evidence map›Paper›PMID 26790728›Full record

ArticleLipids in health and disease2016

Apolipoprotein E polymorphism modulation of asymmetric dimethylarginine in hypertensive patients is determined by renal function.

Mauro Sergio Martins Marrocos, Andrei Alkmin Teixeira, Beata Marie Quinto, Silmara de Melo Carmona, Mariana Kuniyoshi, Cassio Jose Rodrigues, Maria Aparecida Dalboni, Silvia Manfredi, Maria Eugênia Canziani, Marcelo Costa Batista

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
0.4field-weighted citation impact, top 31% 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, 1 synthesis or guideline pooled it, 3 citations in OpenAlex.

  1. Pooled it
  2. Trial
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

10 authors at 2 institutions in 2 countries.

Mauro Sergio Martins MarrocosNephrology Division, Universidade Federal de São Paulo, R. Pedro de Toledo, 781 14 .andar, Vila Clementino, São Paulo, CEP, 04039-032, Brazil. msmarrocos@gmail.com.
Andrei Alkmin TeixeiraNephrology Division, Universidade Federal de São Paulo, R. Pedro de Toledo, 781 14 .andar, Vila Clementino, São Paulo, CEP, 04039-032, Brazil. andreialkmin@uol.com.br.
Beata Marie QuintoNephrology Division, Universidade Federal de São Paulo, R. Pedro de Toledo, 781 14 .andar, Vila Clementino, São Paulo, CEP, 04039-032, Brazil. marie.quinto@unifesp.br.
Silmara de Melo CarmonaNephrology Division, Universidade Federal de São Paulo, R. Pedro de Toledo, 781 14 .andar, Vila Clementino, São Paulo, CEP, 04039-032, Brazil. melosilmara@ymail.com.
Mariana KuniyoshiNephrology Division, Universidade Federal de São Paulo, R. Pedro de Toledo, 781 14 .andar, Vila Clementino, São Paulo, CEP, 04039-032, Brazil. mari.kuni@gmail.com.
Cassio Jose RodriguesNephrology Division, Universidade Federal de São Paulo, R. Pedro de Toledo, 781 14 .andar, Vila Clementino, São Paulo, CEP, 04039-032, Brazil. cjorodrigues@uol.com.br.
Maria Aparecida DalboniNephrology Division, Universidade Federal de São Paulo, R. Pedro de Toledo, 781 14 .andar, Vila Clementino, São Paulo, CEP, 04039-032, Brazil. dalboni@unifesp.br.
Silvia ManfrediNephrology Division, Universidade Federal de São Paulo, R. Pedro de Toledo, 781 14 .andar, Vila Clementino, São Paulo, CEP, 04039-032, Brazil. silvia.hemod@hrim.com.br.
Maria Eugênia CanzianiNephrology Division, Universidade Federal de São Paulo, R. Pedro de Toledo, 781 14 .andar, Vila Clementino, São Paulo, CEP, 04039-032, Brazil. dialisefor@yahoo.com.br.
Marcelo Costa BatistaNephrology Division, Universidade Federal de São Paulo, R. Pedro de Toledo, 781 14 .andar, Vila Clementino, São Paulo, CEP, 04039-032, Brazil. marcelocbatista@uol.com.br.
Universidade Federal de São Paulo · BRHospital Israelita Albert Einstein · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEndothelial dysfunction is considered an early step of atherosclerotic vascular disease. Asymmetric dimethylarginine (ADMA), the main endogenous inhibitor of nitric oxide synthase (NOS), plays a critical role in the process of atherosclerosis in a uremic environment. Increased plasma ADMA not only works as a cardiovascular morbidity biomarker but it is also involved in the genesis of atherosclerosis in renal disease. Considering the relationships of apolipoprotein E(ApoE) polymorphism with LDL cholesterol (LDL-C) levels and coronary risk, it is possible that it brings on susceptibility to endothelial dysfunction and atherogenesis seen on uremia.

methodsSix hundred twenty patients were stratified according to glomerular filtration rate (GFR) estimated by Chronic Kidney Disease Epidemiology Collaboration (CKDEPI) formula: group I > 60 mL/min, group II ≤ 60 mL/min and > 15 mL/min, and group III ≤ 15 mL/min or in hemodialysis. Polymorphic ApoE analysis was performed by polymerase chain reaction amplification (PCR). Plasma ADMA levels were measured by high performance liquid chromatography (HPLC). Groups were compared on clinical and laboratory characteristics as well as allele and genotype distribution towards.

resultsThe ε2 allele of ApoE was present in 62 (10.3 %) patients, ε3 allele in 581 (96.2 %), and ε4 allele in 114 (18.9 %). Their distribution among the 3 groups was uniform. Such uniformity was not observed when we considered endothelial function measured by asymmetric dimethylarginine. In group III, the frequency of ε4 allele was significantly lower in the third tertile compared with the first tertile (14.7 versus 53.3 %, P = 0.000; Pearson chi-square). In groups I and II, there was no difference in allele frequency according to ADMA levels. This association remained significant even after confouding factors corrections (OR 0.329, 95 % CI 0.155 - 0.699, P = 0.004).

conclusionsThe results of this study shows that the frequency of ε4 allele of ApoE is significantly lower among hypertensive patients on hemodialysis with the highest levels of ADMA. Uremia is capable of determining lower plasma ADMA levels in hypertensive ε4 allele carriers.

Indexed as

Kidney Function TestsPolymorphism, GeneticAllelesApolipoproteins EArginineDemographyFemaleHumansHypertensionKidneyLogistic ModelsMaleMiddle AgedRacial GroupsRenal Replacement TherapyApolipoproteins EArginineN,N-dimethylarginine

Identifiers

PMID26790728
PMCPMC4719742
OpenAlexW2276472352

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.