extremely low in advanced renal failure; the concentration is normal or increased, however, in patients with early to moderate renal failure, in whom hypocalcaemia, secondary hyperparathyroidism, and defective bone mineralisation are often present.4Furthermore, treatment with 1 cx,25-dihydroxy or 1 oc-hydroxy vitamin D3 might alleviate skeletal pain, increase serum calcium concentration, suppress secondary hyperparathyroidism, and improve the skeletal lesions of osteitis fibrosa; results in patients with osteomalacia, however, were disappointing.5The question remains, therefore, whether another metabolite of vitamin D, important for normal bone structure, is affected in renal failure.24,25-Dihydroxy vitamin D may possibly play a part in normal bone formation.2Our findings show that production of this metabolite is already impaired in early stages of renal failure.If low serum concentrations of 24,25-dihydroxy vitamin D are causally related to the osteomalacia of chronic renal failure, treatment with both 1,25-dihydroxy and 24,25-dihydroxy vitamin D may be needed to prevent and heal renal osteodystrophy.
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Worth et al. (1980) studied this question.
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