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Background Endothelial microparticles are associated with chronic kidney disease ( CKD ) and complement activation. We hypothesized that the complement pathway is activated in patients with CKD via endothelial microparticles and that complement activation correlates with endothelial dysfunction in CKD . Methods and Results We analyzed complement data of 30 healthy subjects, 30 patients with stage III / IV CKD , and 30 renal transplant recipients with stage III / IV CKD , evaluating the potential correlation of complement fragments with brachial artery flow–mediated dilation, Chronic Kidney Disease Epidemiology Collaboration glomerular filtration rate, and urinary albumin/creatinine ratio. Endothelial microparticles were characterized via proteomic analysis and compared between study groups. Complement fragment Ba was significantly increased in CKD and post–kidney transplant CKD . Plasma Ba levels correlated significantly with lower brachial artery flow–mediated dilation, lower Chronic Kidney Disease Epidemiology Collaboration glomerular filtration rate, and higher urinary albumin/creatinine ratio. Factor D levels were significantly higher in the plasma microparticles of patients with CKD versus healthy controls. Plasma microparticles isolated from patients with CKD and containing factor D activated the alternative pathway in vitro. Conclusion The alternative complement pathway is activated in CKD and correlates with endothelial dysfunction and markers of CKD . Future studies are needed to evaluate whether endothelial microparticles with increased factor D play a pathologic role in CKD ‐associated vascular disease. Clinical Trial Registration URL : http://www.clinicaltrials.gov . Unique identifier: NCT 02230202.