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Updated: Jun 3, 2026
Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Microparticles and Kawasaki disease: a marker of vascular damage?
Serena Guiducci1, Laura Ricci, Eloisa Romano
1Department of BioMedicine, Division of Rheumatology, DENOThe Centre, University of Florence, Florence, Italy. s.guiducci@hotmail.com
Background:
Microparticles (MPs) are increased in diseases characterised by endothelial injury. Kawasaki disease (KD) damages the endothelium provoking life-threatening involvement of coronary arteries.
Objectives:
To compare KD MPs vs. controls. METHODS. Thirty KD and 20 controls were enrolled. MPs were stained with monoclonal antibodies against platelets, endothelial cells (EC), monocytes, T and B cells, neutrophils, and quantified by FACS.
Results:
The total number of MPs was significantly increased in KD versus controls (193x105±0.6x105 vs. 94x105±0.9x105 million/ml plasma p=0.01) and vs. KD after IVIG therapy (132x105±0.4x105million/ml plasma p=0.01). EC and T cells were the major source of MPs in KD (72x105±1x105 vs. 3x105±0.9x105million/ml plasma for T cells p=0.005; 76x105±0.7x105 vs. 45x105±0.4x105 million/ml plasma for EC p<0.02) followed by MPs derived from platelets (13x105±0.3x105 vs. 3x105±0.9x105 million/ml plasma p=0.028). Cell-derived MPs B were 17x105±0.4x105 vs. 20x105±0.8x105million/ml plasma in controls (p=0.7). No significant differences were observed in KD MPs derived from monocytes and neutrophils. After IVIG administration, a significant decrease of MPs derived from platelets (3x105±0.2x105 million/ml plasma p=0.03), EC (9x105±0.4x105 million/ml plasma p=0.01), T cells (72x105±1x105 million/ml plasma p=0.02) and B cells (7x105±0.3x105 million/ml plasma p=0.02) was observed.
Conclusions:
The number of KD MPs is significantly increased and EC and T cells are the major source. MPs may develop from endothelial damage and cell activation. Their role as markers of disease activity or as contributors to endothelial derangement in KD has to be further investigated.
Insights
Microparticle levels are significantly elevated in Kawasaki disease (KD) patients, primarily originating from endothelial cells and T cells. Intravenous immunoglobulin therapy effectively reduces these microparticles, suggesting their role in disease activity.
Area of Science:
- Cardiovascular Research
- Immunology
- Pediatric Medicine
Background:
- Microparticles (MPs) are biomarkers of endothelial injury, frequently elevated in conditions like Kawasaki disease (KD).
- KD is a critical pediatric illness causing endothelial damage and potential coronary artery complications.
Purpose of the Study:
- To quantitatively compare microparticle levels in KD patients versus healthy controls.
- To identify the cellular origins of microparticles in KD.
- To assess the impact of intravenous immunoglobulin (IVIG) therapy on microparticle levels in KD.
Main Methods:
- Flow cytometry (FACS) was used to quantify MPs.
- Monoclonal antibodies targeted platelets, endothelial cells (EC), monocytes, T cells, B cells, and neutrophils.
- Thirty KD patients and 20 controls were analyzed.
Main Results:
- Total MPs were significantly higher in KD patients compared to controls (193x10^5 vs. 94x10^5 million/ml, p=0.01).
- Endothelial cells (76x10^5) and T cells (72x10^5) were the predominant sources of MPs in KD.
- IVIG therapy significantly reduced MPs from platelets, EC, T cells, and B cells.
Conclusions:
- Kawasaki disease is associated with a significant increase in microparticles, mainly from endothelial cells and T cells.
- MPs may serve as indicators of endothelial damage and disease activity in KD.
- Further research is needed to elucidate the precise role of MPs in KD pathogenesis and as therapeutic markers.
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