Urine Calcium
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Calcium is one of the most abundant minerals in the human body. It has roles as the primary component of the transmembrane electrical gradient, in bone mineralization, and as an enzyme cofactor in the coagulation cascade. The body normally keeps serum and intracellular calcium levels under tight control through bone resorption and urinary excretion. The reference ranges of urinary calcium are dependent on the diet and the ability of its intestinal absorption.
Males: 25-300 mg/24-hour specimen*
Females: 20-275 mg/24-hour specimen*
Hypercalciuria: >350 mg/24-hour specimen
(*These levels are reflective of individuals with average, unrestricted calcium intake, which is 600-800 mg/day.)
Furthermore, accurate interpretation of urine calcium concentration should be done in relation to glomerular filtrate (GF), considering the following equation:
UCa(mg/100 ml GF) = [UCa (mg/dl) X Serum Creatinine (mg/dl)] / Urine Creatinine (mg/dl)
A value exceeding 0.16 mg/100 ml GF suggests an intense osteoclastic activity and bone resorption, and it is useful is evaluating renal stone disease and high turnover osteoporosis. [1]
For persons with an average daily calcium intake of 600-800 mg, daily calcium excretion is normally as follows:
Males: 25-300 mg
Females: 20-275 mg
The following conditions increase daily calcium excretion:
Osteolytic bone metastases
Myeloma
Vitamin D and A intoxication [3]
Distal renal tubular acidosis
Idiopathic hypercalciuria
Thyrotoxicosis
Hepatolenticular degeneration
Malignancy (breast, bladder)
Osteitis deformans
Immobilization
The following drugs are also sources of increased daily calcium excretion:
Calcium salts
Acetazolamide
Cholestyramine
Corticosteroids
Dihydrotachysterol
Initial diuretic use – Eg, furosemide
Excessive litium (via inducing hyperparathyroidism) [3]
Excesive administration of PTH
Absorptive hypercalciuria (increased calcium absorption by the gut leading to high excretion of calcium in the urine) may be reduced with dietary restriction. This distinguishes these patients from those whose hypercalciuria has resulted from hyperthyroidism, hyperparathyroidism, or Paget disease, as well as from persons with “renal leak” calciuria (which occurs in renal tubular acidosis). [4]
The following conditions decrease daily calcium excretion:
Osteomalacia
Osteoblastic bone metastases
Steatorrhea
Hypocalciuric hypercalcemia (Familial hypocalciuric hypercalcemia) [6]
Gitelman syndrome
Bartter syndrome
Daily calcium excretion can also be reduced by the following drugs:
Aspirin
Bicarbonate
Chronic diuretic use (eg, thiazides, chlorthalidone)
Estrogens
Indomethacin
Lithium (well-controlled doses)
Neomycin
Oral contraceptives
For further reading, please see the Medscape Reference topic Hypercalciuria.
Collection details are as follows:
Container/tube: Plastic 10-mL urine tube (Supply T068) or a clean, plastic aliquot container with no metal cap or glued insert
Specimen volume: 10 mL; mark the total 24-hour volume on the requisition and on the specimen container
Specimen stability: Refrigerated (preferred), frozen, and ambient 7 days
Collection instructions are as follows:
24-hour collection, 24-hour volume required
No preservative
Refrigerate specimen within 4 hours of completion of 24-hour collection
For multiple collections, the addition of preservative or application of temperature controls must occur within 4 hours of completion of the collection
It is recommended that urine specimens should be collected in containers containing low concentration of acids (most communly HCl) to avoid precipitation of calcium salts (eg, calcium oxalate). When such containers/acids are used, patients and laboratories should be carefull regarding their safety when handling and/or mixing the specimen. Also, the measured concentration should be corrected to acount for volume dilution by the acid solution. [1]
When specimens are collected without acid solutions, they must be acidified for 1 hour before testing and carefully mixed. [1]
Calcium is one of the most abundant minerals in the human body. It has roles as the primary component of transmembrane electrical gradient, in bone mineralization, and as an enzyme cofactor in the coagulation cascade. The body normally keeps serum and intracellular calcium levels under tight control through bone resorption, removal from the kidneys, and excretion from the feces.
Evaluation of urine calcium excretion levels can aid in the differential diagnosis of recurrent renal calculi, as well as in the differentiation of familial hypocalciuric hypercalcemia from asymptomatic primary hyperparathyroidism.
Preferable specimens for urine calcium evaluation are 24-hour urine collections (rather than spot urine) using containers with an acid preservative. Creatinine should be determined on every specimen in order to be certain that the collection was adequate. Volume depletion may hinder urine calcium measurement.
In patients with hypoparathyroidism who are undergoing treatment with vitamin D and calcium supplementation, urine calcium concentration should be followed as an important variable. In this condition, a marked elevation in urine calcium concentration may be seen, as there would be no parathyroid hormone–associated increase in calcium reabsorption. Titrate the patient’s dose of vitamin D so that urine calcium does not increase to greater than 350 mg/day. This usually involves a below-normal serum calcium level that is nonetheless high enough to prevent symptoms.
Knowing the patient’s calcium intake is important in the differential diagnosis of idiopathic hypercalciuria; a great deal of variation in normal calcium excretion occurs in association with the dietary calcium level.
Attempting to use an absolute criterion in the diagnosis of hypercalciuria is problematic, because this criterion will be arbitrary, will probably result in the inclusion of some normal individuals in the diagnosis, and may cause some patients with abnormal calcium homeostasis or abnormal renal tubular calcium handling to be overlooked. Nonetheless, urine calcium excretion in most healthy men and women who consume an average of 600-1000 mg of elemental calcium daily is, respectively, less than 300 mg/day and less than 250 mg/day. The excretion values are higher in cases of idiopathic hypercalciuria.
Urine calcium excretion in most normal men and women with restricted calcium intake (400 mg/day) is, respectively, less than 250 mg/day and less than 200 mg/day. Urine calcium excretion is typically below 100 mg/day in patients with familial hypocalciuric hypercalcemia, despite the presence of hypercalcemia. [7, 8]
Urine calcium excretion is normal in about one third of patients with hyperparathyroidism.
The ratio of urine calcium to urine creatinine (UCa/UCr ratio) can be used to demonstrate the extent of calcium excretion. As such, hypercalciuria is defined as a UCa/UCr ratio of more than 0.20 and more than 0.57 in men and women, respectively.
This test is not usually required to diagnose hyperparathyroidism (which can be diagnosed using serum calcium and parathyroid hormone values), but it can aid in the evaluation of renal stones. The test may also help in excluding the presence of familial hypocalciuric hypercalcemia in hypercalcemic patients.
For the diagnosis of hypercalciuria, good correlation exists between UCa/UCr ratios (in random, single-voided urine specimens) and 24-hour calcium excretion values.
Carl Burtis, Edward Ashwood, David Brunes. Mineral and Bone Metabolism. Elsevier Inc. Tietz’s Textbook of Clinical Chemistry and Molecular Diagnostics. 4th. Elsevier Inc; 2006. 1904-1905. [Full Text].
Halse J, Greenspan S, Cosman F, Ellis G, Santora A, Leung A, et al. A Phase 2, Randomized, Placebo-Controlled, Dose-Ranging Study of the Calcium-Sensing Receptor Antagonist MK-5442 in the Treatment of Postmenopausal Women With Osteoporosis. J Clin Endocrinol Metab. 2014 Aug 28. jc20134009. [Medline].
William Clarke. Calcium Biology and Disorders. AACC Press. Contemporary Practice of Clinical Chemistry. 2nd. AACC Press; 2011. 514-519. [Full Text].
Leslie SW, Taneja A. Hypercalciuria. 2018 Jan. [Medline]. [Full Text].
Yang B, Dissayabutra T, Ungjaroenwathana W, Tosukhowong P, Srisa-Art M, Supaprom T, et al. Calcium Oxalate Crystallization Index (COCI): an Alternative Method for Distinguishing Nephrolithiasis Patients from Healthy Individuals. Ann Clin Lab Sci. 2014 Summer. 44(3):262-71. [Medline].
Gallagher JC, Smith LM, Yalamanchili V. Incidence of hypercalciuria and hypercalcemia during vitamin D and calcium supplementation in older women. Menopause. 2014 Jun 16. [Medline].
Pietrow PK, Karellas ME. Medical management of common urinary calculi. Am Fam Physician. 2006 Jul 1. 74(1):86-94. [Medline].
Reynolds TM. ACP Best Practice No 181: Chemical pathology clinical investigation and management of nephrolithiasis. J Clin Pathol. 2005 Feb. 58(2):134-40. [Medline]. [Full Text].
Alina G Sofronescu, PhD, NRCC-CC, FACB Assistant Professor, Board Certified Clinical Chemist, Medical Director of Clinical Chemistry Laboratory, Department of Pathology and Microbiology, University of Nebraska Medical Center
Alina G Sofronescu, PhD, NRCC-CC, FACB is a member of the following medical societies: American Association for Clinical Chemistry, Canadian Society of Clinical Chemists
Disclosure: Nothing to disclose.
Eric B Staros, MD Associate Professor of Pathology, St Louis University School of Medicine; Director of Clinical Laboratories, Director of Cytopathology, Department of Pathology, St Louis University Hospital
Eric B Staros, MD is a member of the following medical societies: American Medical Association, American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology
Disclosure: Nothing to disclose.
Imaad Razzaque, MD Resident Physician, Department of Internal Medicine, St Louis University School of Medicine
Disclosure: Nothing to disclose.
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