Background Mortality risk for people with chronic kidney disease is substantially greater than that for the general population, increasing to a 7-fold greater risk for those on dialysis therapy. Higher body mass index, generally due to higher energy intake, appears protective for people on dialysis therapy, but the relationship between energy intake and survival in those with reduced kidney function is unknown. Study Design Prospective cohort study with a median follow-up of 14.5 (IQR, 11.2-15.2) years. Setting & Participants Blue Mountains Area, west of Sydney, Australia. Participants in the general community enrolled in the Blue Mountains Eye Study (n = 2,664) who underwent a detailed interview, food frequency questionnaire, and physical examination including body weight, height, blood pressure, and laboratory tests. Predictors Relative energy intake, food components (carbohydrates, total sugars, fat, protein, and water), and estimated glomerular filtration rate (eGFR). Relative energy intake was dichotomized at 100%, and eGFR, at 60 mL/min/1.73 m 2. Outcomes All-cause and cardiovascular mortality. Measurements All-cause and cardiovascular mortality using unadjusted and adjusted Cox proportional regression models. Results 949 people died during follow-up, 318 of cardiovascular events. In people with eGFR < 60 mL/min/1.73 m2 (n = 852), there was an increased risk of all-cause mortality (HR, 1.48; P = 0.03), but no increased risk of cardiovascular mortality (HR, 1.59; P = 0.1) among those with higher relative energy intake compared with those with lower relative energy intake. Increasing intake of carbohydrates (HR per 100 g/d, 1.50; P = 0.04) and total sugars (HR per 100 g/d, 1.62; P = 0.03) was associated significantly with increased risk of cardiovascular mortality. Limitations Under-reporting of energy intake, baseline laboratory and food intake values only, white population. Conclusions Increasing relative energy intake was associated with increased all-cause mortality in patients with eGFR < 60 mL/min/1.73 m2. This effect may be mediated by increasing total sugars intake on subsequent cardiovascular events.