Abstract
Calcitriol, 1,25(OH)2D3, has been reported to have a beneficial effect on bone histology in patients with predialysis chronic renal failure; however, such treatment involves a risk of hypercalcemia. To investigate the effects of 1,25(OH)2D3 and 22-oxacalcitriol (OCT) on the progression of histologic deterioration, we administered intraperitoneal 1,25(OH)2D3 or OCT, three times a week, to rats with adriamycin-induced progressive renal failure, from the 10th week after the induction of ADR-induced nephropathy. The rats were divided into the following groups: (1) high-dose 1,25(OH)2D3, 0.2 μg/kg (group D3-0.2); (2) low-dose 1,25(OH)2D3, 0.04 μg/kg (group D3-0.04); (3) high-dose OCT, 0.2 μg/kg (group OCT-0.2); (4) low-dose OCT, 0.04 μg/kg (group OCT-0.04); and (5) ADR-induced nephropathy (group ADR). The death rate at week 20 in group D3-0.2 was 50%, significantly higher than the death rates in the other groups, except for group D3-0.04 (P <.05). The serum creatinine and blood urea nitrogen levels were the highest in group D3-0.2, although the difference was not significant. In contrast, in groups OCT-0.2 and OCT-0.04, tubular changes and interstitial volume were smaller than in groups D3-0.2 and D3-0.04 (P <.05). Although calcium deposits increased in group D3-0.2, the difference was not significant. Glomerular expression of transforming growth factor-β1 (TGF-β1) expression was less in groups OCT-0.2 and OCT-0.04 than in groups D3-0.2 and D3-0.04 (P <.05). Glomerular fibronectin expression was less in group OCT-0.2 than in groups D3-0.2 and ADR (P <.05). Tubulointerstitial expression of TGF-β1 was greater in group D3-0.2 than in group ADR and greater in group D3-0.04 than in group OCT-0.04 (P <.05). We conclude that a high dose of 1,25(OH)2D3 accelerated the progressive renal deterioration of ADR-induced nephropathy, and, as a result, OCT was able to attenuate renal histologic lesions. (J Lab Clin Med 2002;140:242-9)
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