To develop an animal model of nephrolithiasis similar to the pattern of human renal stone disease, we adopted a protocol of administration of stone substrates along with induction of renal tubular injuries. Male Wister rats f3ed with 3% ammonium
oxalate containing chows with or without additional 40 mg/kg/day of gentamicin for 8 days were compared with those fed with normal chows. On dissecting microscopic examination, rats receiving oxalate and gendtamicin showed more crystals and plaques than ratsreceiving oxalate only, both in 15 days and 23 days after feeding, and most of the crystals were located at renal papilla. Average score of crystal abundance was 0.4, 1.15, respectively in rats receiving oxalate only and oxalate plus gentamicin after 15 days of feeding, and 0.9 and 1.55, respectively after 22 dyas. Little crystals were found in rats fed with normal chow with or without gentamicin. Urinary excretion of tubular epithelial brush border enzyme, gamma-glutamyl transpeptidase9ggt), wasincreased by gentamicin administration whereas creatinine clearance rate was not changed. Urinary excretion of oxalate was unchanged, but calcium and uric acid was markedly decreased in rats fed with oxalate and formed crystals, and citrate andmagnesium excretion was also decreased. These results indicate that administration of oxalate along with inducing renal tubular damages by subccutaneous injection of gentamicin seems to form crystals and plaques in the kidney more rapidly andabndantly than feeding with oxalate alone.
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