Low-grade systemic inflammation is an important potential factor in the pathogenesis of insulin resistance in end-stage renal disease (ESRD). Insulin resistance and diabetes, characterized by impaired skeletal muscle glucose uptake or excess hepatic glucose production, are in turn relevant contributors to morbidity and mortality in ESRD patients. Oxidative stress is increased in ESRD, in conservative therapy as well as hemodialysis treatment. Recent evidence suggests that oxidative stress contributes, at least in part, to both inflammation and insulin resistance by modulating the production of proinflammatory cytokines and adipokines in monocytes and in adipose tissue. This review focuses on the pathogenesis of inflammation and oxidative stress, and the effects of their interplay on insulin resistance in ESRD.