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Updated: May 30, 2026

Dynamic Multiparameter Platelet Function Assessment Using a Capacitive Biosensor
Published on: May 2, 2025
Influence of renal function and platelet turnover on the antiplatelet effect of aspirin
Morten Würtz1, Lise N Wulff, Erik L Grove
1Department of Cardiology, Aarhus University Hospital, Skejby, Denmark.
Insights
Increased immature platelets may reduce aspirin
Area of Science:
- Cardiology
- Nephrology
- Hematology
Background:
- Kidney disease is a known risk factor for cardiovascular events.
- Investigating factors affecting antiplatelet therapy is crucial for managing cardiovascular risk in patients with kidney disease.
Purpose of the Study:
- To examine how renal function and platelet turnover impact aspirin's antiplatelet efficacy in coronary artery disease patients.
- To explore the relationship between renal function, von Willebrand factor, and platelet aggregation.
Main Methods:
- 124 patients with coronary artery disease and varying renal function were studied.
- Aspirin's antiplatelet effect was measured using VerifyNow Aspirin assay and multiple electrode aggregometry (MEA).
- Renal function, von Willebrand factor, and immature platelet counts were assessed.
Main Results:
- Renal function did not significantly alter aspirin's antiplatelet effect.
- Impaired renal function correlated with higher von Willebrand factor levels.
- Immature platelet count positively correlated with platelet aggregation measured by MEA.
Conclusions:
- Elevated immature platelet counts may contribute to a reduced antiplatelet response to aspirin.
- Moderate renal impairment is linked to increased von Willebrand factor but not diminished aspirin efficacy.
Introduction:
Kidney disease predisposes to cardiovascular events. This study investigated the influence of renal function and platelet turnover on the antiplatelet effect of aspirin in patients with coronary artery disease.
Materials And Methods:
We included 124 aspirin-treated patients with coronary artery disease and normal to moderately reduced renal function. All tests were performed one hour after aspirin ingestion. Renal function was assessed using creatinine, estimated glomerular filtration rate (eGFR), and cystatin C. The antiplatelet effect of aspirin was evaluated using the VerifyNow Aspirin assay and multiple electrode aggregometry (MEA, Multiplate) induced by collagen (1.0 μg/mL) and arachidonic acid (1.0 mmol/L). Von Willebrand factor was measured as a marker of endothelial dysfunction. Platelet turnover was evaluated by measurements of immature, reticulated platelets.
Results:
Renal function did not influence the antiplatelet effect of aspirin evaluated by MEA (r=-0.2-0.09, p=0.03-0.77) or the VerifyNow (r=-0.12-0.11, all p-values>0.1). In contrast, renal function correlated inversely with von Willebrand factor levels (r(creatinine)=0.48, p<0.0001; r(eGFR)=-0.46, p<0.001; r(cystatin C)=0.54, p<0.0001). The number of immature platelets correlated with platelet aggregation according to MEA (r=0.20-0.39, all p-values<0.03), but not according to VerifyNow (r=-0.07, p=0.50).
Conclusions:
A reduced antiplatelet effect of aspirin may be explained by an increased number of immature platelets. Moderately impaired renal function was associated with high levels of von Willebrand factor, but not with a reduced antiplatelet effect of aspirin.
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