Calcium is the fifth most common element in the body. It is a fundamental element necessary to form electrical gradients across membranes, an essential cofactor for many enzymes, and the main constituent in bone. Under normal physiologic conditions, the concentration of calcium in serum and in cells is tightly controlled. Calcium is excreted in both urine and feces. Ordinarily about 20% to 25% of dietary calcium is absorbed and 98% of filtered calcium is reabsorbed in the kidney. Traffic of calcium between the gastrointestinal tract, bone, and kidney is tightly controlled by a complex regulatory system that includes vitamin D and parathyroid hormone. Sufficient bioavailable calcium is essential for bone health. Excessive excretion of calcium in the urine is a common contributor to kidney stone risk.
Increased urinary calcium excretion (hypercalciuria) is a known contributor to kidney stone disease and osteoporosis. Many cases are genetic (often termed "idiopathic"). Previously such patients were often divided into fasting versus absorptive hypercalciuria depending on the level of urine calcium in a fasting versus fed state, but the clinical utility of this approach is now in question. Overall, the risk of stone disease appears increased when 24-hour urine calcium is >250 mg in men and >200 mg in women. Thiazide diuretics are often used to reduce urinary calcium excretion, and repeat urine collections can be performed to monitor the effectiveness of therapy.
Known secondary causes of hypercalciuria include hyperparathyroidism, Paget disease, prolonged immobilization, vitamin D intoxication, and diseases that destroy bone (such as metastatic cancer or multiple myeloma).
Urine calcium excretion can be used to gauge the adequacy of calcium and vitamin D supplementation, for example in states of gastrointestinal fat malabsorption that are associated with decreased bone mineralization (osteomalacia).