S. W. STANBURY, M.D., F.R.C.P.
The pathogenesis of azotemic osteodystrophy is still uncertain. The demonstration of impaired intestinal absorption of calcium (1, 2), the occurrence of rickets and osteomalacia (3, 4), and their cure by large amounts of vitamin D are all compatible with an acquired insensitivity to the biological effects of vitamin D (1-5). Hypocalcemia when present is associated with reduced osseous responsiveness to the calcemic action of exogenous parathyroid hormone (6), a functional abnormality also found in simple vitamin D deficiency (7). A degree of secondary hyperparathyroidism is to be expected with vitamin D deficiency, but the osseous manifestations of parathyroid activity are
STANBURY SW. The Treatment of Renal Osteodystrophy. Ann Intern Med. 1966;65:1133–1138. doi: 10.7326/0003-4819-65-5-1133
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Published: Ann Intern Med. 1966;65(5):1133-1138.
Endocrine and Metabolism, Metabolic Bone Disorders, Nephrology, Parathyroid Disorders.
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