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24R, 25‐Dihydroxyvitamin D 3 ameliorates the high‐turnover bone diseases without suppressing parathyroid function in chronic renal failure in rats
Author(s) -
KAZAMA Junichiro J,
WA Masafumi FUKAGAWA,
YI Hung,
KUMAGAI Miki,
YAMATO Hideyuki,
TANIGUCHI Nobuyuki,
GEJYO Fumitake,
ARAKAWA Masaaki,
OZAWA Hidehiro,
KUROKAWA Kiyoshi
Publication year - 1996
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1111/j.1440-1797.1996.tb00114.x
Subject(s) - medicine , endocrinology , parathyroid hormone , bone remodeling , hyperparathyroidism , secondary hyperparathyroidism , renal function , calcium
Summary: To evaluate the effect of 24R,25‐dihydroxyvitamin D 3 (24,25D) on uraemic bone disease, we treated the model rats of mild renal failure either with 0.5 μg/kg bodyweight (BW) of 24,25D, or with 5 μg/kg BW of 24,25D, or with 0.01 μg/kg BW of 1,25‐dihydroxyvitamin D 3 (1,25D), or with 0.01 μg/kg BW of 1,25D and 0.5 μg/kg BW of 24,25D, or with vehicle alone, given orally for 16 weeks. the examination of bone histology revealed extreme acceleration of bone turnover and decreased trabecular bone volume with elevated serum parathyroid hormone (PTH) level in vehicle‐treated uraemic rats compared with those of sham‐operated rats. Treatment with 24,25D (5 μg/kg BW) not only ameliorated high‐turnover bone disease as with 1,25D, but also prevented the reduction of trabecular bone volume without any changes of serum PTH levels, suggesting the possible direct effect of 24,25D on the bone. Our data suggest 24,25D may be another useful agent for the treatment of high‐turnover bone disease caused by secondary hyperparathyroidism in chronic renal failure, with less suppression of parathyroid function.