Purpose of review
Regulation of calcium homeostasis during a lifetime is a complex process reflecting a balance among intestinal calcium absorption, bone calcium influx and efflux, and renal calcium excretion. Perturbations can result in hypocalcemia or hypercalcemia and adaptations in calcium handling must occur during growth and aging.
Study of the calcium sensing receptor in the thick ascending limb of Henle and TRPV5 in the distal tubule continues to provide insights into regulation of renal calcium excretion. Hypercalcemia-induced secretion of calcitonin via activation of the calcium-sensing receptor may protect against the development of hypercalcemia. A calcilytic was shown to increase serum calcium by decreasing renal calcium excretion. Ezrin, a cross-linking protein important for renal phosphate handling, is also involved in the regulation of intestinal calcium absorption. Increased 1,25-hydroxyvitamin D (1,25D) values were shown to protect against the development of hypocalcemia by increasing calcium efflux and decreasing calcium influx in bone. Finally, fibroblast growth factor 23 stimulation, which should result in suppression of 1,25D, was shown to be prevented in a model of vitamin D deficiency in which maintenance of 1,25D is important in minimizing hypocalcemia.
Recent information has provided new insights on how intestinal, bone and renal mechanisms are regulated to maintain calcium homeostasis.