We evaluated the possibility of using the urinary concentrations of tryptophan metabolites such as kyn-urenine (KYN) and kynurenic acid (KYNA) for monitoring cadmium (Cd) exposure and detecting early effects of its action in the kidney. For this purpose, we analyzed correlations between urinary excretion of both metabolites, Cd concentration and the activity of isoenzyme B of N-acetyl-ß-D-glucosaminidase (NAG-B), recognized as one of the most sensitive markers of Cd nephrotoxicity. The study was conducted on rats using an experimental model, corresponding to human environmental and occupational exposure to Cd. The rats were administered 5 and 50 mg Cd/l of drinking water for 24 weeks. The administration of Cd resulted in a marked dose-dependent increase in KYN and KYNA elimination. Regression analysis revealed a linear correlation between urinary Cd concentration and KYN or KYNA excretion as well as between urinary NAG-B activity and KYN or KYNA elimination. We hypothesize that metabolites of tryptophan via kynurenine pathway such as KYN and especially KYNA can be used to monitor chronic exposure to Cd.