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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.
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 exists in 3 states in the body; bound to protein, bound to small anions, and in the free (ionized) state. The concentration of serum calcium in the ionized state is regulated by parathyroid hormone (PTH) and 1,25 dihydroxy vitamin D.
Circulating calcium is excreted by glomerular filtration and reabsorbed in the proximal tubules. Calcium reabsorption in the proximal tubule is affected by tubular sodium concentration, whereas PTH induces calcium uptake in the distal tubule and the collecting duct. Excess is excreted in the urine and the feces.
Because PTH increases renal tubular reabsorption of calcium, one would expect patients with hyperparathyroidism to be hypocalciuric. However, highly urinary calcium/creatinine ratios were found in most hyperparathyroid patients, and less frequently in patients with hypercalcemia due to other causes.
Calcium/creatinine ratio of random urine specimens may be used to detect hypercalciuria in patients suspected of having metabolic bone disease or other abnormalities of calcium metabolism.
0-12 months: <2,100 mg/g
13-24 months: <450 mg/g
25 months-5 years: <350 mg/g
6-10 years: <300 mg/g
11-18 years: <260 mg/g
> or =19 years: <220 mg/g
Increased urinary excretion of calcium accompanies hyperparathyroidism, vitamin D intoxication, diseases that destroy bone (such as multiple myeloma), metastasis from prostatic cancer, and following 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's 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 mg to 800 mg of calcium per day, the normal daily excretion of calcium is:
-Males: 25 mg to 300 mg
-Females: 20 mg to 275 mg
The normal urine calcium/creatinine ratio is <220 mg/g.
No significant cautionary statements
1. Metz JP: Determining urinary calcium/creatinine cutoffs for the pediatric population using published data. Ann Clin Biochem 2006 Sep;43(Pt 5):398-401
2. Saleh F, Jorde R, Sartberg J, et al: The relationship between blood pressure and serum parathyroid hormone with special reference to urinary calcium excretion: the Tromso Study. J Endocrinol Invest 2006 Mar;29(3):214-220
3. Christensen SE, Nissen PH, Vestergaard P, et al: Discriminative power of three indices of renal calcium excretion for the distinction between familial hypocalcuric hypercalemia and primary hyperparathyroidism: a follow-up study on methods. Clin Endocrinol 2008 Nov;69(5):713-720