Clinical meaning
Serum calcium is tightly regulated between 8.5-10.5 mg/dL through the interplay of three hormones. Parathyroid hormone (PTH), released from the parathyroid glands in response to low ionized calcium detected by calcium-sensing receptors (CaSR), raises serum calcium by stimulating osteoclast-mediated bone resorption, increasing renal calcium reabsorption in the distal convoluted tubule, and activating 1-alpha-hydroxylase in the proximal tubule to convert 25-hydroxyvitamin D to active 1,25-dihydroxyvitamin D (calcitriol). Calcitriol increases intestinal calcium and phosphorus absorption via upregulation of calbindin transport proteins. Calcitonin, secreted by thyroid parafollicular C-cells in response to hypercalcemia, inhibits osteoclast activity and promotes renal calcium excretion. The NP must integrate this axis when evaluating calcium disorders: primary hyperparathyroidism (autonomous PTH secretion), secondary hyperparathyroidism (CKD-driven), hypoparathyroidism (post-surgical or autoimmune), and vitamin D deficiency states.