Urinary sodium levels, reflecting salt intake, have been linked to the development of cardiovascular disease and chronic kidney disease (CKD). Excessive sodium consumption may exacerbate CKD, through indirect mechanisms, such as blood pressure (BP) elevation or via direct nephrotoxic effects. However, the extent to which these associations vary by ethnicity remains unclear. This study included 5,655 participants with CKD G2–4 from two prospective CKD cohorts: the CRIC study in the United States and the KNOW-CKD study in South Korea. The primary exposure was 24-hour urinary sodium excretion. The primary outcome included CKD progression, defined as ≥50% decline of baseline estimated glomerular filtration rate or initiation of kidney failure with replacement therapy. Cause-specific models were employed to evaluate to the relationship between 24-hour urinary sodium excretion and the risk of CKD. Causal mediation analysis was conducted to quantify the extent to which systolic blood pressure mediated this relationship. Over a median follow-up of 5.43 years (39,085 person-years), the primary outcome occurred in 1,896 patients, with an incident rate of 48.5 per person years. Participants in the highest quartile exhibited a greater risk of CKD progression compared to those in the lowest quartile. The adjusted HRs (95% CIs) for CKD progression were 1.28 (1.06–1.55) in the CRIC cohort and 2.08 (1.33–3.24) in the KNOW-CKD cohort. Mediation analysis revealed that systolic BP accounted for 24% of the observed effect on CKD progression in the CRIC cohort, compared to only 1% in the KNOW-CKD cohort. Higher urinary sodium excretion was associated with increased CKD progression in both cohorts. However, mechanistic pathways differed by ethnicity: systolic BP mediated a greater effect in CRIC, whereas KNOW-CKD showed a more direct, BP-independent effect. These findings suggest ethnic and physiological differences in sodium-related kidney injury and underscore the need for personalized dietary interventions in CKD management.