Haemodiafiltration elicits less platelet activation compared to haemodialysis

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Abstract

Background

Mortality in patients with end-stage renal disorders is often a consequence of cardiovascular complications. Renal replacement therapies may contribute to this morbidity by promoting cellular activation. In renal failure patients peripheral blood samples were investigated for platelet and endothelial cell activation markers to compare the effects of haemodiafiltration (HDF) and haemodialysis (HD).

Methods

Overall 28 patients were included in the study. Platelet P-selectin and leukocyte - platelet heterotypic aggregates were studied by flow cytometry. Soluble P- and E-selectin values were determined by ELISA, while von Willebrand factor (vWF) antigen levels were measured by immunoturbidimetry. Statistical analysis was done by the SPSS v22 software.

Results

Platelet surface P-selectin was below 3.0 % in healthy controls, but it was higher during the dialysis after 4 h, 8 % and 14.3 % in HDF and HD, respectively. Monocyte-platelet heterotypic aggregates were significantly elevated after 4 h in both treatments, up to 69.2 % in HDF and to 82.9 % in HD. Soluble P-selectin levels were also significantly elevated by the end of both treatment procedures ( p < 0.001), vWF antigen values, however, showed elevation only during HD treatment.

Conclusions

The attenuated platelet activating effects of HDF compared to HD may contribute to a less unfavourable vascular effect in this treatment modality.

Electronic supplementary material

The online version of this article (doi:10.1186/s12882-016-0364-x) contains supplementary material, which is available to authorized users.

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Most cited references 27

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C-reactive protein induces human peripheral blood monocytes to synthesize tissue factor.

J. Čermák, N Key, R R Bach … (1993)

The acute inflammatory response is frequently accompanied by serious thrombotic events. We show that C-reactive protein (CRP), an acute-phase reactant that markedly increases its serum concentration in response to inflammatory stimuli, induced monocytes to express tissue factor (TF), a potent procoagulant. Purified human CRP in concentrations commonly achieved in vivo during inflammation (10 to 100 micrograms/mL) induced a 75-fold increase in TF procoagulant activity (PCA) of human peripheral blood mononuclear cells (PBM), with a parallel increase in TF antigen levels. CRP-induced PCA was completely blocked by a monoclonal antibody against human TF but not by irrelevant murine IgG. Dot blot analysis showed a significant increase of TF mRNA after 4 hours of incubation with CRP, followed by a peak of PCA within 6 and 8 hours. Actinomycin D and cycloheximide blocked CRP-stimulated PCA, suggesting that de novo TF protein synthesis was required. Endotoxin (LPS) contamination of CRP was excluded as the mediator of TF synthesis because: (1) CRP was Limulus assay negative; (2) induction of TF PCA by CRP was not blocked by Polymyxin B, in contrast to LPS-induced PCA; (3) antihuman CRP IgG inhibited CRP-induced PCA, but not LPS-induced PCA; (4) CRP was able to stimulate TF production in LPS-pretreated PBM refractory to additional LPS stimulation; and, (5) unlike LPS, CRP was incapable of inducing TF in human umbilical vein endothelial cells. We suggest that CRP-mediated TF production in monocytes may contribute to the development of disseminated intravascular coagulation and thrombosis in inflammatory states.

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Monitoring of inflammation in patients on dialysis: forewarned is forearmed.

Friedo W Dekker, Peter Stenvinkel, Enrique J. Carrero … (2011)

Current evidence about the effects of inflammation on the outcomes of patients with advanced chronic kidney disease (CKD) generally originates from single measurements of inflammatory biomarkers. Patients with CKD, however, are exposed to persistent low-grade inflammation and levels of serum inflammatory markers are subjected to a substantial variability over time, being influenced by multiple processes, such as transient infections, comorbidities, and the intermittent stimulus of dialysis. Understanding and evaluating inflammation in the context of its time-dependent oscillations in renal disease fluctuation is, therefore, important. Nevertheless, the relationship between longitudinal inflammatory variation and risk prediction has so far been addressed in only a few studies, not all of which have been sufficiently powered. Consequently, uncertainty exists about how to interpret the findings of these studies in the clinical setting. The purpose of this Review is to explore the reasons and implications of variability in levels of inflammatory biomarkers in patients with uremia, specifically focusing on C-reactive protein (CRP) measurements. We also discuss the value of repeated versus single measurements of inflammation in the clinical setting and provide solutions to reduce both sample size and intraindividual variability in hypothetical, randomized controlled trials aimed at reducing CRP levels in patients undergoing hemodialysis.

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Increased platelet and leukocyte activation as contributing mechanisms for thrombosis in essential thrombocythemia and correlation with the JAK2 mutational status.

J Reverter, E Rodrigo, Francisco Cervantes Constantino … (2006)

The mechanisms accounting for the increased risk of thrombosis in patients with essential thrombocythemia (ET) are not well known. The aim of the present study was to ascertain the role of platelet and leukocyte activation in the thrombosis of ET. The activation status of platelets and leukocytes was assessed by flow cytometry studies in 49 patients with ET (22 with previous thrombosis and 27 without a history of thrombosis) and in a group of age- and sex-matched healthy individuals. The assessment included platelet P-selectin expression (measured both at baseline and after stimulation with ADP, thrombin, arachidonic acid (AA), and collagen), platelet-neutrophil and platelet-monocyte complexes, determination of CD11b in the neutrophils and monocytes, and expression of tissue factor in the monocytes (mTF). The JAK2 V617F mutation was studied and correlated with platelet and leukocyte activation. As compared with controls, ET patients had significantly higher values of baseline P-selectin and thrombin- and AA-induced platelet P-selectin expression, as well as higher platelet-neutrophil and platelet-monocyte complexes, neutrophil CD11b expression and baseline mTF expression. Platelet P-selectin, monocyte CD11b, and lipopolysaccharide-induced mTF expression was significantly higher in ET patients with a history of thrombosis than in patients without thrombosis. Patients with the JAK2 V617F mutation or thrombosis showed higher baseline and AA-induced platelet P-selectin expression than did those without thrombosis. These results would support a role for platelet and monocyte activation in the thrombosis of ET. In these patients, the presence of the JAK2 V617F mutation is associated with higher platelet activation.

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Author and article information

Contributors

János Kappelmayer: +36-52-340-006 , kappelmayer@med.unideb.hu

Journal

Journal ID (nlm-ta): BMC Nephrol

Journal ID (iso-abbrev): BMC Nephrol

Title: BMC Nephrology

Publisher: BioMed Central (London )

ISSN (Electronic): 1471-2369

Publication date (Electronic): 13 October 2016

Publication date PMC-release: 13 October 2016

Publication date Collection: 2016

Volume: 17

Electronic Location Identifier: 147

Affiliations

[1 ]Department of Nephrology, University of Debrecen, Debrecen, Hungary

[2 ]Department of Laboratory Medicine, University of Debrecen, Nagyerdei krt. 98, Debrecen, Hungary

[3 ]MTA-DE Vascular Biology, Thrombosis and Hemostasis Research Group, Hungarian Academy of Sciences, Debrecen, Hungary

Article

Publisher ID: 364

DOI: 10.1186/s12882-016-0364-x

PMC ID: 5064778

PubMed ID: 27737645

SO-VID: a0d1985d-f8f9-48b7-b536-1d1eca5eaa54

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 25 May 2016

Date accepted : 11 October 2016

Custom metadata

ScienceOpen disciplines: Nephrology

Keywords: esrd,haemodiafiltration,haemodialysis,monocyte-platelet aggregate,p-selectin

Data availability:

ScienceOpen disciplines: Nephrology

Keywords: esrd, haemodiafiltration, haemodialysis, monocyte-platelet aggregate, p-selectin

Haemodiafiltration elicits less platelet activation compared to haemodialysis

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Abstract

Background

Methods

Results

Conclusions

Electronic supplementary material

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Karger: Nephrology

Most cited references 27

C-reactive protein induces human peripheral blood monocytes to synthesize tissue factor.

Monitoring of inflammation in patients on dialysis: forewarned is forearmed.

Increased platelet and leukocyte activation as contributing mechanisms for thrombosis in essential thrombocythemia and correlation with the JAK2 mutational status.

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