Calcium absorption decreases with aging, particularly after age 70 yr. We investigated the possibility that this was due to abnormal vitamin D metabolism by studying 10 normal premenopausal women (group A), 8 normal postmenopausal women within 20 yr of menopause (group B), 10 normal elderly women (group C), and 8 elderly women with hip fracture (group D) whose ages (mean ± SD) were 37 ± 4, 61 ± 6, 78 ± 4, and 78 ± 4 yr respectively. For all subjects, serum 25-hydroxyvitamin D [25(OH)D] did not decrease with age, but serum 1,25-dihydroxyvitamin D [1,25(OH)2D], the physiologically active vitamin D metabolite, was lower (P = 0.01) in the elderly (groups C and D; 20 ± 3 pg/ml) than in the nonelderly (groups A and B; 35 ± 4 pg/ml). The increase of serum 1,25(OH)D after a 24-h infusion of bovine parathyroid hormone fragment 1-34, a tropic agent for the enzyme 25(OH)D 1α-hydroxylase, correlated inversely with age (r = -0.58; p < 0.001) and directly with glomerular filtration rate (r = 0.64; P < 0.001). The response was more blunted (P = 0.001) in elderly patients with hip fracture (13 ± 3 pg/ml) than in elderly controls (25 ± 3 pg/ml). We conclude that an impaired ability of the aging kidney to synthesize 1,25(OH)2D could contribute to the pathogenesis of senile osteoporosis.
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