Endothelial microparticles (EMPs) are vesicles derived from cell membranes, which contain outsourced
phosphatidylserine and express adhesion molecules, such as
cadherin, intercellular
cell adhesion molecule-1 (ICAM-1),
E-selectin, and
integrins. EMPs are expressed under physiological conditions and continue circulating in the plasma. However, in pathologic conditions their levels increase, and they assume a pro-inflammatory and pro-
coagulant role via interactions with monocytes; these effects are related to the development of
atherosclerosis. Chronic kidney dysfunction (CKD) characterizes this dysfunctional scenario through the accumulation of uremic solutes in the circulating plasma, whose toxicity is related to the development of
cardiovascular diseases. Therefore, this review aims to discuss the formation of EMPs and their biological effects in the uremic environment. Data from previous research demonstrate that
uremic toxins are closely associated with the activation of inflammatory
biomarkers, cardiovascular dysfunction processes, and the release of EMPs. The impact of a decrease in circulating EMPs in clinical studies has not yet been evaluated. Thus, whether MPs are
biochemical markers and/or therapeutic targets has yet to be established.