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Platelet reactivity in patients with chronic kidney disease and hemodialysis

  • Philipp Mourikis
  • Carolin Helten
  • Lisa Dannenberg
  • Thomas Hohlfeld
  • Johannes Stegbauer
  • Tobias Petzold
  • Bodo Levkau
  • Tobias Zeus
  • Malte Kelm
  • Amin PolzinEmail author
Article

Abstract

End stage renal disease requiring hemodialysis (HD) is frequent and coronary artery disease (CAD) is a common comorbidity. It is associated with bleeding and ischemic events. Platelet reactivity is a well-known determinant of both. However, the impact of HD due to end stage chronic kidney disease (CKD) on platelet reactivity is unknown. Therefore in this study, we evaluated platelet reactivity during hemodialysis in patients with CKD and coronary artery disease. 22 patients with CKD, HD and CAD were included in this study. Light transmission aggregometry (LTA) and flow cytometry were used for evaluating platelet function immediately before and 2 h after initiation of HD. Arachidonic acid-induced maximum of aggregation (MoApre HD: 27.36% ± 25.23% vs. MoAduring HD: 28.05% ± 23.50%, p value = 0.822), adenosine diphosphate (ADP)-induced platelet aggregation (MoApre HD: 65.36% ± 12.88% vs. MoAduring HD: 61.55% ± 17.17%, p-value = 0.09) and collagen-induced platelet aggregation (MoApre HD: 62.18% ± 18.14% vs. MoAduring HD: 64.82% ± 18.31%, p-value = 0.375) were not affected by HD. P-selectin expression was significantly lower after 2 h of HD (pre HD: 31.56% ± 18.99%, during HD: 23.97% ± 15.28%, p = 0.026). In this pilot study, HD did not enhance platelet aggregation. Baseline platelet reactivity was decreased during HD.

Keywords

Aggregation Chronic kidney disease Coronary artery disease Hemodialysis Platelets 

Abbreviations

ADP

Adenosine diphosphate

AA

Arachidonic acid

CAD

Coronary artery disease

CKD

Chronic kidney disease

FACS

Fluorescence activated cell sorting

HD

Hemodialysis

LTA

Light transmission aggregometry

MoA

Maximum of aggregation

PRP

Platelet rich plasma

Notes

Author contributions

PM and LD designed the study, analyzed and interpreted data and wrote the manuscript. CH, TH collected data and revised the manuscript. BL, TP, TZ, MK, JS and AP supervised the study and revised the manuscript.

Funding

This work was supported by the Forschungskommission of the Medical Faculty of the Heinrich Heine University (No. 16-2014 to A.P.; No. 46-2016 to L.D.) and by the German Research Foundation (PO 2247/1-1 to A.P.)

Compliance with ethical standards

Conflict of interest

All authors declare that they have no conflicts to disclose.

Ethics approval

The study conformed to the Declaration of Helsinki and was approved by the University of Düsseldorf Ethics Committee.

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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2019

Authors and Affiliations

  • Philipp Mourikis
    • 1
  • Carolin Helten
    • 1
  • Lisa Dannenberg
    • 1
  • Thomas Hohlfeld
    • 2
  • Johannes Stegbauer
    • 3
  • Tobias Petzold
    • 4
  • Bodo Levkau
    • 5
  • Tobias Zeus
    • 1
  • Malte Kelm
    • 1
  • Amin Polzin
    • 1
    • 6
    Email author
  1. 1.Division of Cardiology, Pulmonology, and Vascular MedicineHeinrich Heine University Medical Center DusseldorfDusseldorfGermany
  2. 2.Institute for Pharmacology and Clinical PharmacologyHeinrich Heine UniversityDusseldorfGermany
  3. 3.Division of NephrologyHeinrich Heine University Medical Center DusseldorfDusseldorfGermany
  4. 4.Medizinische Klinik und Poliklinik I, Klinikum der Universität München, Ludwig-Maximilians- University MunichMünchenGermany
  5. 5.Institute of Pathophysiology, West German Heart and Vascular CenterUniversity Hospital Essen, University of Duisburg-EssenEssenGermany
  6. 6.Klinik für Kardiologie, Pneumologie und Angiologie, Universitätsklinikum DüsseldorfDüsseldorfGermany

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