Evidence map›Paper›PMID 28747177›Full record

ArticleBMC cardiovascular disorders2017

Acute coronary syndrome and acute kidney injury: role of inflammation in worsening renal function.

Jorge Ortega-Hernández, Rashidi Springall, Fausto Sánchez-Muñoz, Julio-C Arana-Martinez, Héctor González-Pacheco, Rafael Bojalil

Open access · goldAbstract read
In one paragraph

Article in BMC cardiovascular disorders, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Article
  7. Observational
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Observational
  20. Observational
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

6 authors at 2 institutions in 1 country.

Jorge Ortega-HernándezDepartment of Immunology, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano 1, Sección XVI, Tlalpan, 14080, Mexico City, Mexico.
Rashidi SpringallDepartment of Immunology, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano 1, Sección XVI, Tlalpan, 14080, Mexico City, Mexico.
Fausto Sánchez-MuñozDepartment of Immunology, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano 1, Sección XVI, Tlalpan, 14080, Mexico City, Mexico.
Julio-C Arana-MartinezDepartment of Immunology, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano 1, Sección XVI, Tlalpan, 14080, Mexico City, Mexico.
Héctor González-PachecoCoronary Care Unit, Instituto Nacional de Cardiología Ignacio Chávez, Tlalpan, 14080, Mexico City, Mexico.
Rafael BojalilDepartment of Immunology, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano 1, Sección XVI, Tlalpan, 14080, Mexico City, Mexico. rafaelbojalil@gmail.com.ORCID 0000-0002-5806-3675
Instituto Nacional de Cardiología · MXUniversidad Autónoma Metropolitana · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute Kidney Injury (AKI), a common complication of acute coronary syndromes (ACS), is associated with higher mortality and longer hospital stays. The role of cytokines and other mediators is unknown in AKI induced by an ACS (ACS-AKI), leading to several unanswered questions. The worsening of renal function is usually seen as a dichotomous phenomenon instead of a dynamic change, so evaluating changes of the renal function in time may provide valuable information in the ACS-AKI setting. The aim of this study was to explore inflammatory factors associated to de novo kidney injury induced by de novo cardiac injury secondary to ACS.

methodsOne hundred four consecutive patients with ACS were initially included on the time of admission to the Coronary Unit of the Instituto Nacional de Cardiología in Mexico City, from February to May 2016, before any invasive procedure, imaging study, diuretic or anti-platelet therapy. White blood count, hemoglobin, NT-ProBNP, troponin I, C-reactive protein, albumin, glucose, Na

resultsPositive correlations of ΔCr were found with BUN, admission Cr, GRACE score, IL-1β, IL-6, NT-ProBNP and age, and negative correlations with systolic blood pressure, mean-BP, diastolic-BP and LxA4. In the regression analyses IL-10 and RvD1 had positive non-linear associations with ΔCr. ET-1 had also a positive association. Significant non-linear associations were seen with NT-proBNP, admission Cr, BUN, Na

conclusionInflammation and its components play an important role in the worsening of renal function in ACS. IL-10, ET-1, IL-1β, TnI, RvD1 and LxA4 represent mediators that might be associated with ACS-AKI. IL-6, ET-1, NT-ProBNP might represent crossroads for several physiopathological pathways involved in "de novo cardiac injury leading to de novo kidney injury".

Indexed as

Acute Coronary SyndromeAcute Kidney InjuryAgedBiomarkersCardio-Renal SyndromeCytokinesFemaleHumansInflammationInflammation MediatorsKidneyMaleMexicoMiddle AgedPrognosisProtein Interaction MapsBiomarkersCytokinesInflammation MediatorsAcute coronary syndromeAcute renal injuryCardiorenal crosstalkCytokinesInflammationLipid mediators

Identifiers

PMID28747177
PMCPMC5530514
OpenAlexW2739462844

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.