Hyperuricemia is an important risk factor for vascular inflammation, yet the potential mechanisms of uric acid (UA) in endothelial cells are not well understood. UA has been found to stimulate renin-angiotensin system (RAS) activation in human umbilical vein endothelial cells (HUVECs). (Pro)renin receptor ((P)RR) is widely expressed in endothelial cells and able to induce RAS activation. Whether UA-induced endothelial cell inflammation is via up-regulating (P)RR remained unknown. Primary HUVECs were cultured and treated with UA, under the condition of (P)RR or AT1 silencing. The degree of inflammation in HUVECs was determined by Real-time PCR and monocyte adhesion assay. The protein levels of (P)RR were determined by western blotting or immunofluorescence. Probenecid was used to block UA re-absorption in this study. Adhesion of monocytes to HUVECs was elucidated by microfluidic chip. We found (P)RR is up-regulated in HUVECs following UA stimulation. UA promoted vascular inflammation, which was characterized by up-regulating of cytokines and enhanced monocyte adhesion. Silencing of (P)RR alleviated UA-induced vascular inflammation. Probenecid treatment abolished UA-induced vascular inflammation in HUVECs via suppressing (P)RR up-regulation. This finding was further verified by using microfluidic chip. Our findings indicate that (P)RR plays a critical role in endothelial inflammation in response to UA stimulation.