Diabetes mellitus is a risk factor of chronic kidney disease (CKD); however, the relationship between fasting glucose and CKD remains controversial in non-diabetic population. Therefore, we aimed to evaluate the relationship between genetically predicted fasting glucose and incident CKD in this population. This study included 6,354 participants without diabetes and CKD from the Korean Genome Epidemiology Study. The genetic risk score (GRS9) was calculated using nine genetic variants associated with fasting glucose in previous genome wide association studies. Incident CKD was defined as estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 or proteinuria (≥1+). The causal relationship between fasting glucose and CKD was evaluated using the Mendelian randomization (MR) approach. The GRS9 was strongly associated with fasting glucose (β, 1.01; P < 0.001). During a median follow-up of 11.6 years, 531 (8.4%) CKD events occurred. However, GRS9 was not significantly different between participants with CKD events and those without. After adjusting for confounding factors, fasting glucose was not associated with incident CKD (odds ratio [OR], 0.991; 95% confidence interval [CI], 0.980–1.003; P = 0.139). In the MR analysis, GRS9 was not associated with CKD development (OR per 1 standard deviation increase, 1.179; 95% CI, 0.819–1.696; P = 0.376). Further evaluation using various other MR methods and strict CKD criteria (decrease in the eGFR of ≥ 30% to a value of < 60 mL/min/1.73m2) found no significant relationship between GRS9 and incident CKD. Fasting glucose was not causally associated with CKD development in non-diabetic population.