Evidence map›Paper›PMID 29700922›Full record

ArticleJournal of clinical hypertension (Greenwich, Conn.)2018

The responses of the inflammatory marker, pentraxin 3, to dietary sodium and potassium interventions.

Jia-Wen Hu, Yang Wang, Chao Chu, KeKe Wang, Yu Yan, Wenling Zheng, Qiong Ma, Jian-Jun Mu

Open access · bronzeAbstract read
In one paragraph

Article in Journal of clinical hypertension (Greenwich, Conn.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 29% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Effects of salt intervention on serum levels of Klotho influenced by salt sensitivity.Journal of clinical hypertension (Greenwich, Conn.) · 2020
    Article
  7. Article
  8. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Jia-Wen HuDepartment of Cardiology, First Affiliated Hospital of Medical School, Xi'an Jiaotong University, Xi'an, China.
Yang WangDepartment of Cardiology, First Affiliated Hospital of Medical School, Xi'an Jiaotong University, Xi'an, China.
Chao ChuDepartment of Cardiology, First Affiliated Hospital of Medical School, Xi'an Jiaotong University, Xi'an, China.
KeKe WangDepartment of Cardiology, First Affiliated Hospital of Medical School, Xi'an Jiaotong University, Xi'an, China.
Yu YanDepartment of Cardiology, First Affiliated Hospital of Medical School, Xi'an Jiaotong University, Xi'an, China.
Wenling ZhengDepartment of Cardiology, First Affiliated Hospital of Medical School, Xi'an Jiaotong University, Xi'an, China.
Qiong MaDepartment of Cardiology, First Affiliated Hospital of Medical School, Xi'an Jiaotong University, Xi'an, China.
Jian-Jun MuDepartment of Cardiology, First Affiliated Hospital of Medical School, Xi'an Jiaotong University, Xi'an, China.
First Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pentraxin-3 is a sensitive marker of inflammation that plays dual roles, pathogenic and cardioprotective, in the progression of cardiovascular diseases. Inflammation is intimately involved in salt-induced hypertension. We investigated the responses of pentraxin-3 to sodium and potassium supplementation to elucidate the potential role of pentraxin-3 in salt-induced hypertension. A total of 48 participants from northwest China were enrolled. All participants were maintained on a 3-day normal diet, which was sequentially followed by a 7-day low-sodium diet, a 7-day high-sodium diet, and a 7-day high-sodium plus potassium diet. Plasma concentrations of pentraxin-3 were assessed using ELISA. Plasma pentraxin-3 decreased significantly during the low-salt period compared to baseline (0.57 ± 0.19 ng/mL vs 0.72 ± 0.33 ng/mL, P = .012) and increased during the high-salt period (0.68 ± 0.26 ng/mL vs 0.57 ± 0.19 ng/mL, P = .037). Potassium supplementation inhibited salt-induced increase in pentraxin-3 (0.56 ± 0.21 ng/mL vs 0.68 ± 0.26 ng/mL, P = .015). Ln-transformed pentraxin-3 at baseline was inversely correlated with BMI (r = -.349, P = .02), DBP (r = -.414, P = .005), MAP (r = -.360, P = .017). We found a positive correlation between the ln-transformed concentrations of pentraxin-3 and 24-hour urinary sodium during low and high Na

Indexed as

AgedBiomarkersBlood PressureCardiovascular DiseasesChinaC-Reactive ProteinDietary SupplementsDiet, Sodium-RestrictedFemaleHumansHypertensionInflammationMaleMiddle AgedPentraxinsPotassiumBiomarkersC-Reactive ProteinPentraxinsPotassiumSerum Amyloid P-ComponentSodium, Dietaryinflammationpentraxin-3potassiumsalt intakesalt sensitivity

Identifiers

PMID29700922
PMCPMC8031200
OpenAlexW2799453590

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.