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High-turnover bone due to excess PTH is one of the main types of renal osteodystrophy. In addition to the classic stimuli of PTH secretion such as hypocalcemia and decreased production of active vitamin D, new mechanisms has been suggested. Furthermore, skeletal resistance to PTH, a classic stimulus of PTH secretion in uremia, has been recently revisited as an underlying abnormality.
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Fukagawa et al. (2002) studied this question.
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