Epidemiologic studies show a strong association of low birth weight with hypertension, renal and cardiovascular disease, especially after catch-up growth. Senescence is an important contributor to progression of chronic disease. Developmentally programmed premature senescence may be a link between low birth weight, catch-up growth, and adult disease. Low birth weight was induced by feeding pregnant rats a low protein diet from day 12 of gestation to 10 days post-delivery. Low and normal birth weight male offspring were weaned onto regular or high calorie diets to enhance catch-up growth. Kidneys and hearts of offspring were analyzed for RNA and protein markers of stress-induced senescence (p16, p21, p53, Rb). Markers of mitochondrial stress (p66Shc) and activation of endoplasmic reticulum protein secretion (Ero1) were analyzed as regulators of reactive oxygen species generation. Reactive oxygen species are known to be associated with premature aging. Senescence markers were not different in low or normal birth weight kidneys at birth. During rapid catch-up growth, p16 and p21 increased significantly in low birth weight kidneys and hearts (p < 0.01). Renal p16 levels increased progressively and were significantly higher in low birth weight kidneys at 3 and 6 months (p 0.02). Renal p66Shc and Ero1 were significantly higher in low compared to normal birth weight kidneys at 6 months suggesting reactive oxygen species generation (p 0.03). Low birth weight rats exhibit accelerated senescence in kidneys and hearts after rapid catch-up growth, a likely important link between early growth and subsequent hypertension, renal and cardiovascular disease.