The population in the Western world is aging. In 1996 those aged 60 years and over formed 21% of the EU population, by 2022 this proportion will have risen to 27%. Based on current trends a third of the EU population could be 60 years of age and over by the age 2050. Epidemiological studies suggest that even in the absence of other risk factors (e.g. diabetes, hypertension, hypercholesterolemia), advanced age itself significantly increases cardiovascular morbidity by promoting the development of atherosclerosis and by impairing normal cellular functions. One of the most prominent organs affected by aging is the kidney. There is evidence that age-associated phenotypic changes may be an important cause of renal failure. We propose that vascular oxidative stress and inflammation are generalized phenomena during senescence, which importantly contribute to the morphological and functional changes in the aging kidney. The present review focuses on some of the mechanisms by which advanced age may promote vascular oxidative and nitrosative stress and the possible downstream mechanisms by which reactive oxygen and nitrogen species may impair vascular and renal function in aging.