**1. Introduction**

Calcium is one of the essential minerals in the human body being enrolled in various metabolic functions. About 99% of the total body's calcium is present in bone, but the remaining fraction that is present in plasma or the intracellular compartment has a vital role in muscular contraction, normal blood coagulation system, cardiac muscle contractility and rhythm in addition to many other vital functions. Calcium homeostasis requires integration among various organs within the human body such as parathyroid glands, intestine and kidneys. In other words, normal concentration of plasma parathyroid hormone, intact absorptive function of the intestine, proper activation of vitamin D and normal renal re-absorptive and excretory function are all essential to maintain plasma calcium level within the reference range. In patients with chronic kidney disease (CKD), specifically those with advanced stage, there will be an associated progressive impairment of vitamin D activation due to progressive loss of nephrons. This will lead to significant malabsorption of calcium by the intestine with consequent hypocalcemia. This hypocalcemia, in addition to other factors, represents a major stimulus on parathyroid hormone (PTH) secretion by one of two mechanisms that are dependent on the duration of hypocalcemia. In the short term, hypocalcemia will stimulate PTH secretion via G-protein while prolonged hypocalcemia is associated with altered stability of m-RNA-encoding PTH. The pathophysiology of hypocalcemia in patients with chronic kidney disease

is related to two main factors. First, the precipitation of calcium on various body tissues after being complexed with plasma phosphorus that is present in higher concentrations. Second, impaired absorption of calcium at the intestine secondary to the deficient active form of the vitamin (1,25 (OH)2 vitamin D) due to improper activation of vitamin D by the renal cortex. Because of the prolonged stimulation of parathyroid glands by the persistent hypocalcemia in patients with chronic kidney disease, secondary hyperparathyroidism will be an expected associated finding in such patients. So, secondary hyperparathyroidism will ensue with a consequent increase in plasma level of PTH. This condition is commonly encountered in patients with chronic kidney disease especially with advanced stages and has been proposed to be correlated with certain complications commonly seen in such patients including cardiovascular diseases and renal osteodystrophy. For this reason, the prognostic value of PTH in patients with chronic kidney disease has received great emphasis.
