Platelet reactivity in patients with chronic kidney disease and hemodialysis

Abstract

End stage renal disease requiring hemodialysis (HD) is frequent and coronary artery disease (CAD) is a common comorbidity. It is associated with bleeding and ischemic events. Platelet reactivity is a well-known determinant of both. However, the impact of HD due to end stage chronic kidney disease (CKD) on platelet reactivity is unknown. Therefore in this study, we evaluated platelet reactivity during hemodialysis in patients with CKD and coronary artery disease. 22 patients with CKD, HD and CAD were included in this study. Light transmission aggregometry (LTA) and flow cytometry were used for evaluating platelet function immediately before and 2 h after initiation of HD. Arachidonic acid-induced maximum of aggregation (MoApre HD: 27.36%\u2009±\u200925.23% vs. MoAduring HD: 28.05%\u2009±\u200923.50%, p value\u2009=\u20090.822), adenosine diphosphate (ADP)-induced platelet aggregation (MoApre HD: 65.36%\u2009±\u200912.88% vs. MoAduring HD: 61.55%\u2009±\u200917.17%, p-value\u2009=\u20090.09) and collagen-induced platelet aggregation (MoApre HD: 62.18%\u2009±\u200918.14% vs. MoAduring HD: 64.82%\u2009±\u200918.31%, p-value\u2009=\u20090.375) were not affected by HD. P-selectin expression was significantly lower after 2 h of HD (pre HD: 31.56%\u2009±\u200918.99%, during HD: 23.97%\u2009±\u200915.28%, p\u2009=\u20090.026). In this pilot study, HD did not enhance platelet aggregation. Baseline platelet reactivity was decreased during HD.