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May 1969

Calcium, Phosphorus, and Bone in Renal Disease and Transplantation

Author Affiliations

St. Louis; Chicago; St. Louis

From the Renal Division and Endocrinology Division of Washington University School of Medicine and the Jewish Hospital of St. Louis, St. Louis (Drs. Bricker, Slatopolsky, and Avioli), and the Department of Medicine, Michael Reese Hospital and Medical Center, Chicago.

Arch Intern Med. 1969;123(5):543-553. doi:10.1001/archinte.1969.00300150061009

Calcium-phosphate-bone interrelationships become disrupted progressively in advancing renal disease. Parathyroid hormone (PTH) release, normally attuned to calcium homeostasis requirements, becomes dominated by alterations in phosphate balance. With each wave of nephron destruction, there is believed to occur transient hyperphosphatemia, transient hypocalcemia, and a step-wise rise in PTH levels. When the glomerular filtration rate falls below 25 to 30 ml per minute, hyperphosphatemia persists, hypocalcemia tends to persist, and the stimulus to PTH release is exaggerated. Vitamin D resistance contributes both to hypocalcemia (thus to accelerated PTH secretion) and to osteomalacia. In patients receiving long-term hemodialysis, if hyperphosphatemia and hypocalcemia persist, PTH levels may remain high and osteitis fibrosa may progress. Successful renal transplantation typically leads to regression of hyperparathyroidism and restoration of vitamin D sensitivity; however, hyperparathyroidism may regress slowly, and severe hypercalcemia must be guarded against. True autonomy of PTH release apparently occurs rarely in chronic renal disease.

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