Abstract
The history of the use of vitamin D metabolites and analogs in clinical medicine began with their use in renal bone disease following the appreciation that the kidney is the major site of the 1 alpha-hydroxylase of vitamin D. In the presence of advanced renal failure, production of calcitriol is impaired and treatment is viewed conceptually as a hormone replacement therapy. Since then, there has been much interest in the rationale for the use of such compounds in osteoporosis. Arguments have been variously forwarded that osteoporosis is in part due to either a defective 1 alpha-hydroxylase occurring at menopause or in later life or to target tissue resistance to calcitriol; some argue that disturbances in vitamin D metabolism are irrelevant to osteoporosis, being either a consequence of aging or a result, not a cause, of osteoporosis itself. This paper reviews these various issues and explores the differences and similarities between the pathogenesis of renal bone disease and osteoporosis.
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