title: Hypocalcemia may not be essential for the development of secondary hyperparathyroidism in chronic renal failure.
abstract: Hypocalcemia is the main factor responsible for the genesis of secondary hyperparathyroidism in chronic renal disease. Studies with parathyroid cells obtained from uremic patients indicate that there is a shift in the set point for calcium-regulated hormone (parathyroid hormone [PTH] secretion. Studies were performed in dogs to further clarify this new potential mechanism. Hypocalcemia was prevented in uremic dogs by the administration of a high calcium diet. Initially, ionized calcium was 4.79 +/- 0.09 mg/dl and gradually increased up to 5.30 +/- 0.05 mg/dl. Despite a moderate increase in ionized calcium, immunoreactive PTH (iPTH) increased from 64 +/- 7.7 to 118 +/- 21 pg/ml. Serum 1,25(OH)2D3 decreased from 25.4 +/- 3.8 to 12.2 +/- 3.6 pg/ml. Further studies were performed in two other groups of dogs. One group received 150-200 ng and the second group 75-100 ng of 1,25(OH)2D3 twice daily. The levels of 1,25(OH)2D3 increased from 32.8 +/- 3.5 to a maximum of 69.6 +/- 4.4 pg/ml. In the second group the levels of serum 1,25(OH)2D3 after nephrectomy remained normal during the study. Amino-terminal iPTH did not increase in either of the two groups treated with 1,25(OH)2D3. In summary, the dogs at no time developed hypocalcemia; however, there was an 84% increase in iPTH levels, suggesting that hypocalcemia, per se, may not be the only factor responsible for the genesis of secondary hyperparathyroidism.
mesh_terms: D000595:Amino Acid Sequence; D000818:Animals; D002117:Calcitriol / Q000097:blood; D004285:Dogs; D005260:Female; D006962:Hyperparathyroidism, Secondary / Q000209:etiology*; D006996:Hypocalcemia / Q000150:complications*; D007676:Kidney Failure, Chronic / Q000150:complications*; D009392:Nephrectomy; D010281:Parathyroid Hormone / Q000097:blood; D014511:Uremia / Q000150:complications
chemical_list: D010281:Parathyroid Hormone; D002117:Calcitriol