Oxidant stress has been implicated in a number of pathologies associated with uremia and hemodialysis. These patients have an increased incidence of cardiovascular disease, amyloidosis associated with protein modification, and notable changes in both function and structure of many cellular components. Oxidative reactions most frequently involving free radical intermediates play an important role in these processes and participate both directly and indirectly by further amplification of the inflammatory responses or in activation of signaling cascades mediating proliferation, differentiation, and cell death. Proteins and lipids are susceptible to oxidative degradation. These changes can ultimately alter important structural and functional characteristics and lead to pathological changes. This article addresses some of the diverse mechanisms and pathways involved in these changes, and suggests new therapeutic strategies in preventing oxidative damage.