Renal osteodystrophy pathophysiology: Difference between revisions
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Revision as of 15:01, 20 July 2016
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
The mineral content of bone is calcium hydroxyapatite, Ca5(PO4)3(OH). When calcium is being actively resorbed from bone, the phosphate also enters the blood stream. The kidney is the primary means of excreting excess phosphate. Renal osteodystrophy results from an abnormally elevated serum phosphate (hyperphosphatemia) and low serum calcium (hypocalcemia), both of which are due to decreased excretion of phosphate by the damaged kidney, low vitamin D levels or tertiary hyperparathyroidism (a dysfunction of the parathyroid gland due to constant stimulation).