Mörtberg J, et al. - In this descriptive analysis of patients with acute myocardial infarction (AMI), researchers investigated if, despite concurrent antithrombotic treatment, AMI patients with chronic kidney disease (CKD) had more elevated platelet microparticles (PMPs; reflect platelet activation) and endothelial microparticles (EMPs; reflect endothelial activation or dysfunction) vs non-CKD patient. They collected fasting blood samples from 47 patients on dual antiplatelet treatment, who were then stratified by renal function as normal (H; n=19) mean estimated glomerular filtration (eGFR) 88; moderate CKD (CKD3; n = 15) mean eGFR 47; and severe CKD (CKD4–5; n = 13) mean eGFR 20 mL/min/1.73 m². Using flow-cytometry, they determined microparticles (MPs) and then, based on size (< 1.0 μm) and expression of CD41 (GPIIb; PMPs) and CD62E (E-selectin; EMPs), MPs were phenotyped. They also assessed the expression of platelet activation markers P-selectin (CD62P) and CD40ligand (CD154). Among AMI patients, further elevation of PMPs and EMPs from activated platelets and endothelial cell was seen in CKD patients. This implied that in spite of simultaneous antiplatelet treatment, CKD patients had reduced endothelial function and higher platelet activation.