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.
