Impaired urine ammonium excretion is common in chronic kidney disease (CKD) and may identify risk of metabolic acidosis earlier than reductions in serum bicarbonate or pH, and thus may have associations with cardiovascular disease (CVD) outcomes. We evaluated the association of urine ammonium with CVD and kidney outcomes among persons with hypertension and non-diabetic CKD enrolled in a trial of blood pressure reduction. We measured urine ammonium concentration in spot urine specimens collected at baseline among 2092 participants of the Systolic Blood Pressure Intervention Trial (SPRINT) with an eGFR <60 ml/min/1.73m2. We used multivariable-adjusted Cox models to evaluate associations of urine ammonium concentration with the SPRINT primary CVD composite outcome (myocardial infarction, acute coronary syndrome, stroke, heart failure, or CVD death), all-cause mortality, the SPRINT kidney composite outcome (50% kidney function decline, end stage kidney disease, or transplant), and acute kidney injury (AKI). At baseline, the mean (SD) age was 73 (9) years; 40% were female; and 25% were Black participants. The mean (SD) serum bicarbonate was 25.6 (2.8) mmol/L, median (interquartile range, IQR) urine ammonium concentration was 14.4 (9.5, 23.1) mmol/L, and median (IQR) eGFR was 49 (39,55) ml/min/1.73m2. There were 255 CVD composite events, 143 deaths, 63 kidney composite events, and 146 AKI events during a median follow-up of 3.8 years. In multivariable models, each 2-fold higher urinary ammonium concentration was associated with a 26% (95% CI 1.05, 1.52) higher risk of the CVD composite, whereas there was no association with all-cause mortality, the SPRINT kidney composite outcome, or AKI. Among non-diabetic individuals with hypertension and CKD, higher urine ammonium concentration is associated with higher risk of CVD. Further studies are needed to evaluate this association in other cohorts.