The Set Point of Intact Parathyroid Hormone-Ionized Calcium Curve during the Progression of Secondary Hyperparathyroidism among Patients Undergoing Haemodialysis

T Sudhakar¹, Sabitha Kandi², B venugopal², K. Bhagwan Reddy³ and K. V. Ramana^3,

¹Department of Biochemistry, HOD lab in-charge, Apollo Reach Hospital, Karimnagar, Andhra Pradesh

²Department of Biochemistry, Chalmeda Anadrao Institute of Medical Sciences, Karimnagar

³Department of Biochemistry, Prathima Institute of Medical Sciences, Karimnagar

Cite this paper:
T Sudhakar, Sabitha Kandi, B venugopal, K. Bhagwan Reddy and K. V. Ramana. The Set Point of Intact Parathyroid Hormone-Ionized Calcium Curve during the Progression of Secondary Hyperparathyroidism among Patients Undergoing Haemodialysis. American Journal of Medical and Biological Research. 2014; 2(4):87-90. doi: 10.12691/ajmbr-2-4-1

Abstract

The parathyroid gland secretes parathyroid hormone (PTH) which is a key element in the regulation of serum calcium. The PTH elevates serum calcium activities by regulating its action on the bones, kidneys and small intestine. The set point of PTH secretion defines the sensitivity of the parathyroid glands to calcium concentration. Secondary hyperparathyroidism (SHPT) is a common complication of end stage renal disease (ESRD). Ionized calcium is physiologically active form of calcium status of the body and is used for accurately monitoring calcium status in renal diseases. The present study states that the ionized calcium is the set point of secondary hyperparathyroidism undergoing haemodialysis and the range of set point lies between 2.3 – 4.8 mg/dl (0.57 – 1.2 mmol/L). The status of iPTH, set point are frequently monitored in subtotal hyperparathyroidectomy where imaging studies are not beneficial (anatomically situated on postero-lateral surface of thyroid gland) to know the appearance of parathyroid gland.

Keywords:
set point ionized calcium Secondary hyperparathyroidism (SHPT) haemodialysis

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References:

[1]	Brown EM. Extracellular ca+2 sensing, regulation of parathyroid cell function, and role of ca+2 and other ions as extracellular (first) messengers. Physiol Rev. 1991: 71; 371-411.
[2]	Brown EM and Macleod RJ. Extracellular calcium sensing and extracellular calcium signaling. Physiol Rev. 2001:81; 239-297.
[3]	Silver J, Kilav R & Naveh-Many T. Mechanisms of secondary hyperparathyroidism. American Journal of Physiology. 2002: 23: F367-F376.
[4]	Brown EM, Gamba G, Riccardi D et al. Cloning and characterization of an extracellular ca+2 -sensing receptor from bovine parathyroid. Nature. 1993: 366: 575-80. [pub med]
[5]	Chattopadhyay N, Mothal A, Brown EM. The calcium-sensing receptor: Window into the physiology and pathophysiology of mineral ion metabolism. Endocr Rev. 1996; 17: 289-307.
[6]	Saidak Z, Mentaverri R, Brown EM. The role of the calcium-sensing receptor in the development and progression of cancer. Endocr Rev. 2009; 30: 178-95. [pub med]
[7]	Kifor O, Moore FD Jr, Wang P, Goldstein M, Vassilev P et al.,. Reduced immunostaining for the extracellular ca+2 sensing receptor in primary and uremic secondary hyperparathyroidism. J Clin Endocrinol Metab. 1996;81: 1598-1606. [pub med]
[8]	Gogusev J, Duchambon P, Hory B, Giovannini M, Goureau Y et al.,. Depressed expression of calcium receptor in parathyroid gland tissue of patients with hyperparathyroidism. Kidney Int. 1997; 51: 328-36. [pub med]
[9]	Mathias RS, Nguyen HT, Zhang MY, Portole AA. Reduced expression of the renal calcium-sensing receptor in rats with experimental chronic renal insufficiency. J Am Soc Nephrol. 1998; 9: 2067-74. [pub med]
[10]	C.E.Duran, Jose Vicente Torregrosa, Y. ALmaden, A. Canalejo, J. M.Campistol et al.,. Dynamics of calcium-regulated PTH secretion in secondary hyperparathyroidism: comparison between invivo Vs invitro responses. Nefrologia 2010; 30 (1); 73-77.
[11]	Felsenfeld AJ, Llach F. Parathyroid gland function in chronic renal failure. Kidney Int 1993; 43: 771-89. [pub med]
[12]	Felsenfeld AJ, Rodriguez M. The set point of calcium. Another view. Nephrol Dial Transplant. 1996;11: 1722-5.[pub med]
[13]	Goodman W, Salusky IB. Parathyroid gland function and the set point for PTH release: understanding the available data. Nephrol Dial Transplant. 1996:11: 16-8. [pub med]
[14]	Parofitt AM. Relation between parathyroid cell mass and plasma calcium concentration in normal and uremic subjects. Arch Intern Med. 1969; 124: 269-73. [pub med]
[15]	Felsenfeld AJ, Rodriguez M, Aguilera-Tejero E. Dynamics of parathyroid hormone secretion in Health and secondary hyperparathyroidism. Clin J Am Soc Nephrol. 2007: 2: 1283-305. [pub med]
[16]	Buritt MF, Picrides AM. Comparative studies of total and ionized calcium in serum in normal subjects and patients with renal disorders. Mayo Clin Prac 1980; 55: 606-13.
[17]	Gidenne S, Vigezzi JF, Delacour H, Damiano J, Clerc Y. Direct determination or estimated value of plasma ionized calcium: indications and limits. Ann Biol Clin (Paris). 2003: 61 (4): 393-9.
[18]	Robertson WG. Measuremenr of ionized calcium in body fluids-a review. Ann Clin Biochem. 1976; 13 (6): 540-8.
[19]	Soong WJ, Wang HZ, Hwang B. Heparinization of blood decreases ionized calcium concentration. Zhonghua Yi Xue Za Zhi (Taipei). 1991; 47 (5): 331-5.
[20]	Brown EM, Wilkson RE, Eastman RC, Pallota J & Marynick SP. Abnormal regulation of parathyroid hormone release by calcium in secondary hyperparathyroidism due to chronic renal failure. Journal of Clinical Endocrinology and Metabolism. 1993; 76: 1489-94.
[21]	Ramirez JA, Goodman WG, Gornbein J, Menezes C, Moulton L et al.,. Direct invivo comparison of calcium-regulated parathyroid hormone secretion in normal volunteers and patients with secondary hyperparathyroidism. Journal of clinical Endocrinology and Metabolism. 1993; 76: 1489-94.
[22]	Goodman WG, Belin T, Gales B, Juppner H, Segre GV et al.,. Calcium regulated parathyroid hormone release in patients with mild or advanced secondary hyperparathyroidism. Kidney International. 1995; 48: 1553-1558.
[23]	Malberti F, Corradi B, Pagliari, Romanini D, Gazo A, et al.,. The sigmoidal parathyroid hormone-ionized calcium curve and the set point of calcium in hemodialysis and continuous ambulatory peritoneal dialysis. Peritoneal Dialysis International. 1993; 13: (suppl 2): S476-S479.
[24]	Goodman WG, Veldhuis JD, Belin TR, Van Herle AJ, Juppner H at al.,. Calcium sensing by parathyroid glands in secondary hyperparathyroidism. Journal of clinical Endocrinology & Metabolism. 1998: 83: 2765-72.
[25]	Borrego MJ, Felsenfeld AJ, Martin-Malo A, Almaden Y, Concepcion MT et al.,. Evidence for adaptation of the entire PTH-calcium curve to sustained changes in the serum calcium in hemodialysis patients. Nephrology Dialysis and Transplantation. 1997; 12: 505-513.
[26]	Cardinal H, Brossard JH, Roy L, Lepage R, Rousseau L & D’Amour P. the setpoint of parathyroid hormone stimulation by calcium is normal in progressive renal failure. Journal of clinical Endocrinology and Metabolism. 1998; 83: 3839-3844.
[27]	Ritter CS, Finch JL, Slatopolsky EA & Brown AJ. Parathyroid hyperplasia in uremic rats precedes down-regulation of the calcium receptor. Kidney International. 2001; 60: 1737-44.
[28]	Carling T, Rastad J, Szabo E, Westin G & Akerstrom G. Reduced parathyroid vitamin D receptor messenger ribonucleic acid levels in primary and secondary hyperparathyroidism. Journal of Clinical Endocrinology and Metabolism. 2000; 85: 2000-2003.
[29]	Lewin E, Garfia B, Recio FL, Rodriguez M & Olgaard K. Persistent downregulation of calcium-sensing receptor mRNA in rat parathyroids when severe secondary hyperparathyroidism is reversed by isogenic kidney transplantation. Journal of the American Society of Nephrology. 2002; 13: 2110-2116.
[30]	Pahl M, Jara A, Bover J, Rodriguez M & Felsenfeld AJ. The set point of calcium and the reduction of parathyroid hormone in hemodialysis patients. Kidney Interrnational. 1996; 49: 226-231.
[31]	Rodriguez M, Caravaca F, Fernandez E, Borrego MJ, Lorenzo V et al.,. Evidence for both abnormal set point of PTH stimulation by calcium and adaptation to serum calcium in hemodialysis patients with hyperparathyroidism. Journal of bone and mineral research. 1997: 12: 347-355.
[32]	Hardy-Yverneau P, Shenouda M, Moriniere P, Lagallais C, Brazier M et al.,. The dependency of calcium set point on basal plasma calcium in dialysis patients: a better explanation for the discrepancies regarding its link with PTH secretion than methodological differences. Clinical Nephrology. 1998; 50: 236-246.
[33]	Malberti F, Farina M & Imbasciati E. The PTH-Calcium curve and the set point of calcium in primary and secondary hyperparathyroidism. Nephrology Dialysis and Transplantation. 1999; 14: 2398-2406.
[34]	Rodriguez M, Caravaca F, Fernandez E, Borrego MJ, Lorenzo V et al. Evidence for both abnormal set point of PTH stimulation by calcium and adaptation to serum calcium in hemodialysis patients with hyperparathyroidism. Journal of Bone and Mineral Research. 1997:12:347-355.