Evidence map›Paper›PMID 31006081›Full record

Observational studyJournal of nephrology2019

Lipopolysaccharide in systemic circulation induces activation of inflammatory response and oxidative stress in cardiorenal syndrome type 1.

Grazia Maria Virzì, Andrea Breglia, Chiara Castellani, Ghada Ankawi, Chiara Bolin, Massimo de Cal, Vito Cianci, Annalisa Angelini, Giorgio Vescovo, Claudio Ronco

Abstract readObservational Study
PubMed Publisher
In one paragraph

Observational study in Journal of nephrology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
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  10. Endogenous Dysregulation of Thromboinflammatory Biomarkers in End-Stage Renal Disease, and Their Amplification by Heart Failure.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
    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

10 authors at 4 institutions in 2 countries.

Grazia Maria VirzìDepartment of Nephrology, Dialysis and Transplantation, St Bortolo Hospital, International Renal Research Institute Vicenza, Via Rodolfi, 37, 36100, Vicenza, Italy. graziamaria.virzi@gmail.com.
Andrea BregliaIRRIV-International Renal Research Institute Vicenza, Vicenza, Italy.
Chiara CastellaniDepartment of Medicine DIMED, University of Padua Medical School, Padua, Italy.
Ghada AnkawiIRRIV-International Renal Research Institute Vicenza, Vicenza, Italy.
Chiara BolinInternal Medicine, San Bortolo Hospital, Vicenza, Italy.
Massimo de CalDepartment of Nephrology, Dialysis and Transplantation, St Bortolo Hospital, International Renal Research Institute Vicenza, Via Rodolfi, 37, 36100, Vicenza, Italy.
Vito CianciEmergency Department of Arzignano Hospital, Arzignano, Vicenza, Italy.
Annalisa AngeliniDepartment of Medicine DIMED, University of Padua Medical School, Padua, Italy.
Giorgio VescovoInternal Medicine, San Bortolo Hospital, Vicenza, Italy.
Claudio RoncoDepartment of Nephrology, Dialysis and Transplantation, St Bortolo Hospital, International Renal Research Institute Vicenza, Via Rodolfi, 37, 36100, Vicenza, Italy.
International Renal Research Institute of Vicenza · ITUniversity of Padua · ITOspedale San Bortolo · ITOspedale Sant Antonio · IT

Funding

Regione del Veneto RSF N. 303/2009
6 · The paper itself

Abstract

backgroundCardiorenal syndrome type 1 (CRS type 1) is characterized by a rapid worsening of cardiac function leading to acute kidney injury. In this study, we evaluate the role of lipopolysaccharide (LPS) and various inflammatory markers in the developing acute kidney injury (AKI) in acute heart failure (AHF) patients.

methodsWe enrolled 31 AHF patients and 20 CRS type 1 (the cause of AKI was presumed to be related to cardiac dysfunction) and 17 healthy volunteers without AHF, AKI or CKD, as control group (CTR). We assessed levels of LPS, proinflammatory cytokines (TNF-α, IL-6, IL-18), and oxidative stress marker (myeloperoxidase, MPO).

resultsWe observed a significant increase in LPS, TNF-α, IL-6, IL-18 and MPO levels in CRS type 1 and AHF group compared to CTR. LPS levels resulted significantly higher in CRS type 1 patients compared with AHF (118.2 pg/mL, IQR 77.8-217.6 versus 13.5 pg/mL, IQR 12.0-17.0, p = 0.008). We found a cytokines and oxidative stress dysregulation in CRS type 1 patients compared with AHF. Furthermore, we observed a strong positive significant correlation between LPS levels and IL-6 (Spearman's rho = 0.79, p < 0.001), and IL-18 (Spearman's rho = 0.77, p < 0.001) and MPO (Spearman's rho = 0.80, p < 0.001), all confirm by simple linear regression analysis.

conclusionCRS type 1 patients presented an increased level of LPS, pro-inflammatory cytokines, and MPO. Furthermore, there is a direct correlation between LPS and pro-inflammatory cytokines and stress oxidative marker. LPS may play a role in the pathophysiology of CRS type 1 inducing inflammation, oxidative stress and finally kidney damage.

Indexed as

Oxidative StressAcute DiseaseAcute Kidney InjuryAgedAged, 80 and overBiomarkersCardio-Renal SyndromeFemaleHeart FailureHumansInflammationInterleukin-18Interleukin-6LipopolysaccharidesMalePeroxidaseBiomarkersIL18 protein, humanInterleukin-18Interleukin-6LipopolysaccharidesMPO protein, humanPeroxidaseTumor Necrosis Factor-alphaCardiorenal syndromeCytokinesHeart failureInflammationLipopolysaccharideOxidative stress

Identifiers

PMID31006081
OpenAlexW2936967367

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.