Evidence map›Paper›PMID 30823870›Full record

ArticleBMC nephrology2019

Increased concentrations of platelet- and endothelial-derived microparticles in patients with myocardial infarction and reduced renal function- a descriptive study.

Josefin Mörtberg, Kristina Lundwall, Fariborz Mobarrez, Håkan Wallén, Stefan H Jacobson, Jonas Spaak

Abstract read
In one paragraph

Article in BMC nephrology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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

21 citing papers in PubMed.

  1. Article
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  4. Article
  5. Article
  6. Platelets in Renal Disease.International journal of molecular sciences · 2023
    Review
  7. Extracellular vesicles as personalized medicine.Molecular aspects of medicine · 2023
    Review
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  12. Article
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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.

Josefin MörtbergDivision of Nephrology, Department of Clinical Sciences, Danderyd University Hospital, Karolinska Institutet, Stockholm, Sweden. josefin.mortberg@sll.se.ORCID 0000-0001-9139-5711
Kristina LundwallDivision of Cardiovascular Medicine, Department of Clinical Sciences, Danderyd University Hospital, Karolinska Institutet, Stockholm, Sweden.
Fariborz MobarrezRheumatology Unit, Department of Medicine, Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Håkan WallénDivision of Cardiovascular Medicine, Department of Clinical Sciences, Danderyd University Hospital, Karolinska Institutet, Stockholm, Sweden.
Stefan H JacobsonDivision of Nephrology, Department of Clinical Sciences, Danderyd University Hospital, Karolinska Institutet, Stockholm, Sweden.
Jonas SpaakDivision of Cardiovascular Medicine, Department of Clinical Sciences, Danderyd University Hospital, Karolinska Institutet, Stockholm, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPatients with chronic kidney disease (CKD) have a high risk of recurring thrombotic events following acute myocardial infarction (AMI). Microparticles (MPs) are circulating small vesicles shed from various cells. Platelet microparticles (PMPs) reflect platelet activation and endothelial microparticles (EMPs) reflect endothelial activation or dysfunction. Both increase following AMI, and may mediate important biological effects. We hypothesized that AMI patients with CKD have further elevated PMPs and EMPs compared with non-CKD patients, despite concurrent antithrombotic treatment.

methodsWe performed a descriptive study of patients with AMI. Fasting blood samples were acquired from 47 patients on dual antiplatelet treatment. Patients were stratified by renal function: normal (H; n = 19) mean eGFR 88; moderate CKD (CKD3; n = 15) mean eGFR 47, and severe CKD (CKD4-5; n = 13) mean eGFR 20 mL/min/1.73 m

resultsPMPs expressing CD40 ligand were higher in CKD4-5: 210 /μl (174-237); median and interquartile range; vs. group H; 101 /μl (71-134; p < 0.0001) and CKD 3: 142 /μl (125-187; p = 0.006). PMPs expressing P-selectin were higher in CKD4-5 compared with H, but not in CKD3. EMPs were higher in CKD4-5; 245 /μl (189-308) compared with H; 83 /μl (53-140; p < 0.0001) and CKD3; 197 /μl (120-245; p < 0.002).

conclusionsIn AMI patients, PMPs and EMPs from activated platelets and endothelial cell are further elevated in CKD patients. This indicate impaired endothelial function and higher platelet activation in CKD patients, despite concurrent antiplatelet treatment.

Indexed as

Myocardial InfarctionPlatelet ActivationRenal Insufficiency, ChronicBlood CoagulationBlood PlateletsCell-Derived MicroparticlesCorrelation of DataEndothelial CellsEndothelium, VascularFemaleFlow CytometryGlomerular Filtration RateHumansKidney Function TestsMaleMiddle AgedPlatelet Aggregation InhibitorsAcute coronary syndromeChronic kidney diseaseHaemostasisRenal dysfunctionRenal failureThrombosis

Identifiers

PMID30823870
PMCPMC6397450

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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.