Hypocalcemia may not be essential for the development of secondary hyperparathyroidism in chronic renal failure

• Published in: The Journal of clinical investigation Vol. 78; no. 4; pp. 1097 - 1102
• Main Authors: LOPEZ-HILKER, S, GALCERAN, T, YUK-LUEN CHAN, RAPP, N, MARTIN, K. J, SLATOPOLSKY, E
• Format: Journal Article
• Language: English
• Published: Ann Arbor, MI American Society for Clinical Investigation 01.10.1986
• Subjects: Amino Acid Sequence; Animals; Biological and medical sciences; Calcitriol - blood; Dogs; Female; Hyperparathyroidism, Secondary - etiology; Hypocalcemia - complications; Kidney Failure, Chronic - complications; Medical sciences; Nephrectomy; Nephrology. Urinary tract diseases; Nephropathies. Renovascular diseases. Renal failure; Parathyroid Hormone - blood; Renal failure; Uremia - complications; Endocrinopathy; Fissipedia; Carnivora; Urinary system disease; Calcium; Inorganic element; Vertebrata; Chronic; Experimental disease; Metabolic disorder; Mammalia; Renal failure; Dog; Hyperparathyroidism; Hypocalcemia
• ISSN: 0021-9738; 1558-8238
• DOI: 10.1172/JCI112666

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.