AbstractRats received either single oral doses of 0, 25, 50, 100 and 200 mg/kg tris(2,3‐dibromopropyl)phosphate (Tris‐BP) or repeated doses of 50, 100 and 200 mg/kg/day Tris‐BP for 7 days. Urine was collected over a 24‐hr period and subjected to13C‐NMR and biochemical examinations. Tris‐BP produced significant increases of urinary glucose and lactate. Urinary γ‐glutamyitransferase, lactate dehydrogenase and alkaline phosphatase levels were significantly elevated on the first 2 days of post‐treatment. Histopathologically, the kidney exhibited proximal tubular damage at a dose of 200 mg/kg. There was a good correlation among the histopathological, biochemical results, and the13C‐NMR urinary metabolite fingerprints in the assessment of Tris‐BP‐induced renal damage. The abnormal patterns of metabolite excretion suggested that the lesions produced by Tris‐BP were caused by changes in the metabolic function of tubular epithelial cells. The urinary excretion of lactate, enzymes and inhibition of glucose reabsorption from the tubular lumina may be attributed to necrosis and desquama