Effects of 1α-Hydroxyvitamin D3 on Experimental Uremic Renal Osteodystrophy in Rats Induced by Na-Sulfacetylthiazole

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  • OKANO KAZUTOSHI
    Department of Geriatrics, Faculty of Medicine, University of Tokyo
  • NAKAI RUMIKO
    Department of Geriatrics, Faculty of Medicine, University of Tokyo
  • TOMORI TAKASHI
    Department of Geriatrics, Faculty of Medicine, University of Tokyo
  • YOSHIKAWA MASAKI
    Department of Geriatrics, Faculty of Medicine, University of Tokyo

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タイトル別名
  • Effects of 1.ALPHA.-hydroxyvitamin D3 on experimental uremic renal osteodystrophy in rats induced by Na-sulfacetylthiazole.
  • Effects of 1アルファ Hydroxyvitamin D3 on E

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Na-sulfacetylthiazole (SAT), 0.1g/kg body weight as 5% aqueous solution, was injected intraperitoneally to Wistar male rats weighing 200 to 300g, twice a week for 1, 2 and 4 months, while 1 α-hydroxy vitamin D3 (1α-OH-D3) was simultaneously administered orally to a half of the SAT-4 month-treated rats at a daily dose of 0.25αg/kg body weight for the last 19 days of the feeding period. Both blood urea nitrogen (BUN) and serum inorganic phosphorus concentrations were markedly increased and the histological examination of the kidneys of SAT-treated rats revealed interstitial nephritis. Serum calcium level was significantly decreased in the rats treated with SAT for 2 or 4 months. Serum parathyroid hormone (PTH) level as well as the wet weight of parathyroid glands was increased in SAT-treated rats, while simultaneous administration of la-OH-D3 inhibited such increases. Serum 25-hydroxyvitamin D3 (25-OH-D3) was decreased in the rats treated with SAT for 2 months. The X-ray density and calcium content of the femurs of SAT-treated rats were decreased, while simultaneous administration of lα-OH-D3 inhibited such decreases. Tetrachrome stain of the femurs of SAT-4 month-treated rats revealed a marked increase of osteoid contents in the bone cortex, while 1α-OH-D3 inhibited such an increase in osteoid formation. These data indicate that 1α-OH-D3 would be effective for the treatment of uremic renal osteodystrophy, although its detailed mechanism remains to be further clarified.

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