An animal model of calcium oxalate urolithiasis based on a cyclooxygenase 2 selective inhibitor.

Urol Res

Department of Urology, Seoul National University College of Medicine and Clinical Research Institute, Seoul National University Hospital, 28, Yongon-dong, Chongno-gu, 110-744 Seoul, Korea.

Published: December 2005

AI Article Synopsis

  • The study aimed to create a model for kidney stone formation by using a COX-2 selective inhibitor in male Sprague-Dawley rats with renal tubular injury.
  • After feeding the rats a diet high in sodium oxalate for two and four weeks, researchers compared urine and kidney samples from both treated and untreated groups.
  • Results indicated that after four weeks, more crystal formation occurred in rats receiving both oxalate and celecoxib, while the model demonstrated mild kidney injury and increased urinary oxalate excretion.

Article Abstract

Our aim was to develop a stone-forming animal model involving renal tubular injury using a cyclooxygenase 2 selective inhibitor. Male Sprague-Dawley rats fed chow containing 3% sodium oxalate with or without 100 mg/kg celecoxib were compared to animals fed normal chow. Rats were killed after 2 or 4 weeks and the kidneys were harvested for morphological examination. Collections of 24-h urine were made before kidney harvest. After 2 weeks only a few crystals were observed in rats that received oxalate and celecoxib, but after 4 weeks more crystals were observed at the renal papilla than in rats that received only oxalate. Few crystals were found in rats fed normal chow with or without celecoxib. The urinary activities of gamma-glutamyl transpeptidase (GGT) were increased by celecoxib administration whereas creatinine clearance rates were unchanged. In rats fed oxalate, urinary oxalate excretion increased, but calcium excretion decreased. This model using a cyclooxygenase 2 selective inhibitor is a useful stone forming animal model involving mild renal tubular injury together with mild hyperoxaluria.

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http://dx.doi.org/10.1007/s00240-005-0507-1DOI Listing

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