Calcium Disorders

Abstract

The plasma levels of calcium and inorganic phosphate are controlled by homeostatic mechanisms. The plasma level of calcium is particularly tightly controlled. Parathyroid hormone (PTH) raises calcium via actions on: bone cells (osteoclasts and osteocytes) to promote mineral resorption; the renal distal tubule to enhance calcium reabsorption; and renal proximal tubule cells to promote 1,25-dihydroxyvitamin D synthesis. Calcium-sensing receptors lower calcium dependent on plasma membrane expression in cells of: the parathyroid gland to suppress PTH secretion and thus serum PTH levels; the renal cortical thick ascending limb to promote urinary calcium losses; and other tissues including thyroid calcitonin-secreting C-cells and osteoclasts. Hypocalcaemia arises as a consequence of a failure of one of the normal homeostatic mechanisms that act to raise the plasma calcium level. Hypocalcaemia may be symptomatic or asymptomatic. Key early clinical features of hypocalcaemia include perioral or peripheral paresthesiae or numbness, and various manifestations of neuromuscular excitation including carpo-pedal spasm. Later, more severe manifestations of hypocalcaemia include convulsions, including febrile convulsions in children. Dietary calcium requirements for adults are around 1–1.5 g/day, reflecting relatively low levels of intestinal absorption efficiency, even in vitamin D replete individuals. Calcium supplements are of particular benefit in patients with osteoporosis on anti-resorptive medications, which impair calcium release from bone, thereby promoting the risk of hypocalcaemia. Hypercalcemia arises as a consequence of a failure of one or more of the normal homeostatic mechanisms that act to lower the plasma calcium level.