Calcium, Random, Urine
Identification of abnormal physiologic states causing excess or suppressed excretion of calcium (such as hyperparathyroidism), vitamin D abnormality, diseases that destroy bone, prostate cancer, and drug treatment (such as thiazide therapy)
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
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 the urine and the feces.
Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.
No established reference values
Increased urinary excretion of calcium accompanies hyperparathyroidism, vitamin D intoxication, diseases that destroy bone (such as multiple myeloma), metastasis from prostatic cancer, and calcium supplementation.
Patients with absorptive hypercalciuria (increased gut absorption) will have lowered urine calcium with dietary restriction and, therefore, can be differentiated from patients with hypercalciuria caused by hyperparathyroidism, hyperthyroidism, Paget disease, or "renal leak" type of calciuria as seen in renal tubular acidosis.
Thiazide drugs tend to reduce excretion of calcium.
For individuals consuming an average daily intake of 600 to 800 mg of calcium per day, the normal daily excretion of calcium is:
-25 to 300 mg for men
-20 to 275 mg for women
Clinical Reference Provides recommendations for further in-depth reading of a clinical nature
Bijvoet OLM: Kidney function in calcium and phosphate metabolism. In Metabolic Bone Disease. Vol. 1. Edited by LV Avioli, SM Krane. New York, Academic Press, 1977, pp 49-140