Different effects of 22-oxacalcitriol and calcitriol on the course of experimental chronic renal failure.

@article{citeulike:1807162, abstract = {Calcitriol, 1,25(OH)(2)D(3), 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)(2)D(3) and 22-oxacalcitriol (OCT) on the progression of histologic deterioration, we administered intraperitoneal 1,25(OH)(2)D(3) 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)(2)D(3), 0.2 microg/kg (group D(3)-0.2); (2) low-dose 1,25(OH)(2)D(3), 0.04 microg/kg (group D(3)-0.04); (3) high-dose OCT, 0.2 microg/kg (group OCT-0.2); (4) low-dose OCT, 0.04 microg/kg (group OCT-0.04); and (5) ADR-induced nephropathy (group ADR). The death rate at week 20 in group D(3)-0.2 was 50\%, significantly higher than the death rates in the other groups, except for group D(3)-0.04 (P <.05). The serum creatinine and blood urea nitrogen levels were the highest in group D(3)-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 D(3)-0.2 and D(3)-0.04 (P <.05). Although calcium deposits increased in group D(3)-0.2, the difference was not significant. Glomerular expression of transforming growth factor-beta1 (TGF-beta1) expression was less in groups OCT-0.2 and OCT-0.04 than in groups D(3)-0.2 and D(3)-0.04 (P <.05). Glomerular fibronectin expression was less in group OCT-0.2 than in groups D(3)-0.2 and ADR (P <.05). Tubulointerstitial expression of TGF-beta1 was greater in group D(3)-0.2 than in group ADR and greater in group D(3)-0.04 than in group OCT-0.04 (P <.05). We conclude that a high dose of 1,25(OH)(2)D(3) accelerated the progressive renal deterioration of ADR-induced nephropathy, and, as a result, OCT was able to attenuate renal histologic lesions.}, address = {Division of Nephrology and Clinical Research Institute, Department of Internal Medicine, National Kyushu Medical Center, 1-8-1 Jigyohama, Chuo-ku, Fukuoka-city, Fukuoka 810-8563, Japan. hdroom@qmed.hosp.go.jp}, author = {Sanai, T. and Tokumoto, M. and Hirano, T. and Okuda, S. }, citeulike-article-id = {1807162}, issn = {0022-2143}, journal = {J Lab Clin Med}, month = {October}, number = {4}, pages = {242--249}, posted-at = {2007-10-22 17:15:45}, priority = {2}, title = {Different effects of 22-oxacalcitriol and calcitriol on the course of experimental chronic renal failure.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/12389022}, volume = {140}, year = {2002} }

TY - JOUR ID - citeulike:1807162 L3 - citeulike-article-id:1807162 TI - Different effects of 22-oxacalcitriol and calcitriol on the course of experimental chronic renal failure. JF - J Lab Clin Med VL - 140 IS - 4 SP - 242 EP - 249 AD - Division of Nephrology and Clinical Research Institute, Department of Internal Medicine, National Kyushu Medical Center, 1-8-1 Jigyohama, Chuo-ku, Fukuoka-city, Fukuoka 810-8563, Japan. hdroom@qmed.hosp.go.jp SN - 0022-2143 N2 - Calcitriol, 1,25(OH)(2)D(3), 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)(2)D(3) and 22-oxacalcitriol (OCT) on the progression of histologic deterioration, we administered intraperitoneal 1,25(OH)(2)D(3) 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)(2)D(3), 0.2 microg/kg (group D(3)-0.2); (2) low-dose 1,25(OH)(2)D(3), 0.04 microg/kg (group D(3)-0.04); (3) high-dose OCT, 0.2 microg/kg (group OCT-0.2); (4) low-dose OCT, 0.04 microg/kg (group OCT-0.04); and (5) ADR-induced nephropathy (group ADR). The death rate at week 20 in group D(3)-0.2 was 50%, significantly higher than the death rates in the other groups, except for group D(3)-0.04 (P <.05). The serum creatinine and blood urea nitrogen levels were the highest in group D(3)-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 D(3)-0.2 and D(3)-0.04 (P <.05). Although calcium deposits increased in group D(3)-0.2, the difference was not significant. Glomerular expression of transforming growth factor-beta1 (TGF-beta1) expression was less in groups OCT-0.2 and OCT-0.04 than in groups D(3)-0.2 and D(3)-0.04 (P <.05). Glomerular fibronectin expression was less in group OCT-0.2 than in groups D(3)-0.2 and ADR (P <.05). Tubulointerstitial expression of TGF-beta1 was greater in group D(3)-0.2 than in group ADR and greater in group D(3)-0.04 than in group OCT-0.04 (P <.05). We conclude that a high dose of 1,25(OH)(2)D(3) accelerated the progressive renal deterioration of ADR-induced nephropathy, and, as a result, OCT was able to attenuate renal histologic lesions. AU - Sanai, T AU - Tokumoto, M AU - Hirano, T AU - Okuda, S PY - 2002/10// UR - http://view.ncbi.nlm.nih.gov/pubmed/12389022 ER -