Abstract
BACKGROUND: Patients with chronic kidney disease (CKD) have a high risk of recurring thrombotic events following acute myocardial infarction (AMI). Microparticles (MPs) are circulating small vesicles shed from various cells. Platelet microparticles (PMPs) reflect platelet activation and endothelial microparticles (EMPs) reflect endothelial activation or dysfunction. Both increase following AMI, and may mediate important biological effects. We hypothesized that AMI patients with CKD have further elevated PMPs and EMPs compared with non-CKD patients, despite concurrent antithrombotic treatment. METHODS: We performed a descriptive study of patients with AMI. Fasting blood samples were acquired from 47 patients on dual antiplatelet treatment. Patients were stratified by renal function: normal (H; n = 19) mean eGFR 88; moderate CKD (CKD3; n = 15) mean eGFR 47, and severe CKD (CKD4-5; n = 13) mean eGFR 20 mL/min/1.73 m(2). MPs were measured by flow-cytometry and phenotyped according to size (< 1.0 μm) and expression of CD41 (GPIIb; PMPs) and CD62E (E-selectin; EMPs). In addition, expression of platelet activation markers P-selectin (CD62P) and CD40ligand (CD154) were also investigated. RESULTS: PMPs expressing CD40 ligand were higher in CKD4-5: 210 /μl (174-237); median and interquartile range; vs. group H; 101 /μl (71-134; p < 0.0001) and CKD 3: 142 /μl (125-187; p = 0.006). PMPs expressing P-selectin were higher in CKD4-5 compared with H, but not in CKD3. EMPs were higher in CKD4-5; 245 /μl (189-308) compared with H; 83 /μl (53-140; p < 0.0001) and CKD3; 197 /μl (120-245; p < 0.002). CONCLUSIONS: In AMI patients, PMPs and EMPs from activated platelets and endothelial cell are further elevated in CKD patients. This indicate impaired endothelial function and higher platelet activation in CKD patients, despite concurrent antiplatelet treatment.