Whole blood platelet aggregation and release reaction testing in uremic patients.

Biomed Res Int

Department of Pathology, George Washington University Medical Center, 900 23rd Street NW, Washington, DC 20037, USA.

Published: February 2014

Background: Platelet function analysis utilizing platelet-rich plasma and optical density based aggregometry fails to identify patients at risk for uremia associated complications.

Methods: We employed whole blood platelet aggregation analysis based on impedance as well as determination of ATP release from platelet granules detected by a chemiluminescence method. Ten chronic kidney disease (CKD) stage 4 or 5 predialysis patients underwent platelet evaluation. Our study aims to evaluate this platform in this patient population to determine if abnormalities could be detected.

Results: Analysis revealed normal aggregation and ATP release to collagen, ADP, and high-dose ristocetin. ATP release had a low response to arachidonic acid (0.37 ± 0.26 nmoles, reference range: 0.6-1.4 nmoles). Platelet aggregation to low-dose ristocetin revealed an exaggerated response (20.9 ± 18.7 ohms, reference range: 0-5 ohms).

Conclusions: Whole blood platelet analysis detected platelet dysfunction which may be associated with bleeding and thrombotic risks in uremia. Diminished ATP release to arachidonic acid (an aspirin-like defect) in uremic patients may result in platelet associated bleeding. An increased aggregation response to low-dose ristocetin (a type IIb von Willebrand disease-like defect) is associated with thrombus formation. This platelet hyperreactivity may be associated with a thrombotic diathesis as seen in some uremic patients.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3708384PMC
http://dx.doi.org/10.1155/2013/486290DOI Listing

Publication Analysis

Top Keywords

atp release
16
blood platelet
12
platelet aggregation
12
uremic patients
12
platelet
9
arachidonic acid
8
reference range
8
low-dose ristocetin
8
associated bleeding
8
aggregation
5

Similar Publications

The photo-induced CO-releasing properties of the dark-stable complex [RuCl(CO)L] (L = 2-(pyridin-2-yl)quinoxaline) were investigated under 468 nm light exposure in the presence and absence of biomolecules such as histidine, calf thymus DNA and hen egg white lysozyme. The CO release kinetics were consistent regardless of the presence of these biomolecules, suggesting that they did not influence the CO release mechanism. The quinoxaline ligand demonstrated exceptional cytotoxicity against human acute monocytic leukemia cells (THP-1), with evidence of potential DNA damage ascertained by comet assay, while it remained non-toxic to normal kidney epithelial cells derived from African green monkey (Vero) cell lines.

View Article and Find Full Text PDF

Background: We recently demonstrated that large extracellular vesicles (EVs) released by Aβ-loaded microglia and carrying Aβ (Aβ-EVs) propagate synaptic dysfunction in the mouse brain by moving at the axon surface (Gabrielli et al., Brain, 2022; Falcicchia et al., Brain Commun, 2023).

View Article and Find Full Text PDF

Background: Mitochondrial dysfunction is an early and prominent feature of Alzheimer's disease (AD). We have recently published that lower brain mitochondrial DNA copy number (mtDNAcn) is associated with increased risk of AD neuropathological change and reduced cognitive performance. Here, we addressed how mtDNAcn affects cell-type specific phenotypes.

View Article and Find Full Text PDF

Basic Science and Pathogenesis.

Alzheimers Dement

December 2024

Alzheimer's Center at Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.

Background: The blood-brain barrier (BBB) is a crucial regulator of cerebral homeostasis and function. Cerebrovascular endothelial cells (EC) are important components of the BBB, and EC damage and/or dysfunction may result in defects in brain clearance and perfusion, microhemorrhages, inflammation, and neurodegeneration. In addition to EC damage resulting from the presence of amyloid-beta (Aβ) in Alzheimer's Disease (AD) and Cerebral Amyloid Angiopathy (CAA), the presence of cardiovascular risk factors (CVRF) may further exacerbate cerebrovascular function and neurodegeneration.

View Article and Find Full Text PDF

Basic Science and Pathogenesis.

Alzheimers Dement

December 2024

Alzheimer's Center at Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.

Background: Neurofibrillary tangles formed by hyperphosphorylated tau aggregates in the brain are one of the classical hallmarks of Alzheimer's Disease (AD). Tau aggregates have been shown to elicit cytotoxicity, leading to overall neuronal loss and cognitive decline in AD. These aggregates can be transmitted from neurons and glial cells to other brain cells through a process known as tau spreading, and ultimately reach the endothelial cells (ECs) lining the vessel walls, thus, causing dysfunction of the neurovascular unit (NVU), a complex multicellular system surrounding brain vessels.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!