Holy et al. suggest that carbamylated (c)LDL promotes thrombus formation in patients with chronic kidney disease (CKD). They found that LDL isolated from these patients (CKD LDL) had higher levels of carbamylation than LDL from healthy controls. In mice, administration of cLDL or of CKD LDL accelerated arterial thrombus formation compared with administration of native LDL. Moreover, cLDL and CKD LDL, but not native LDL, enhanced platelet aggregation in response to agonists via a mechanism involving phosphorylation of MAPK p38 and translocation of LOX-1 to the cell surface.