Differences in calcium oxalate crystal growth inhibition were studied in normally voided urine (bladder urine) and in urine collected directly from the kidney (kidney urine) in nine dogs. Urine samples were collected before and 10 days after bilateral ureterostomies. Calcium oxalate crystal growth inhibition was measured in a standard seeded crystal growth system. The alcian blue-precipitable material of the urine samples was determined. Significantly lower values were observed in kidney urine than in bladder urine for calcium oxalate crystal inhibition (mean difference, 0.07 +/- 0.02 inhibitor units/mg creatinine; P less than 0.01) and for the alcian blue-precipitable material (mean difference, 0.07 +/- 0.02 mg/mg creatinine; P less than 0.01). We conclude that the bladder adds calcium oxalate crystal growth inhibition to urine. Glycosaminoglycans from the bladder mucosa may be responsible; however, other acidic polymers such as RNA fragments or glycopeptides have been shown to be a constituent of the alcian blue-precipitable material. These are potent inhibitors of calcium oxalate crystal growth, and their participation in the increase of inhibition observed in bladder urine cannot be excluded. Total calcium oxalate crystal growth inhibition present in normally voided urine may be an overestimation of the actual inhibition present at the level of the kidney, where calculi usually form.