Calcitriol (1,25 di-OH Vitamin D)

CPT: 82652
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  • 1,25(OH) Vitamin D
  • 1,25-Dihydroxy Vitamin D
  • 1,25-Dihydroxycholecalciferol
  • Vitamin D, 1,25-Dihydroxy

Special Instructions

This test is not the same as Vitamin D, 25-Hydroxy [081950] (vitamin D3), which must be ordered separately.

Expected Turnaround Time

2 - 4 days

Related Documents

Specimen Requirements


Serum or plasma


0.5 mL

Minimum Volume

0.3 mL (Note: This volume does not allow for repeat testing.)


Red-top tube, gel-barrier tube, green-top (heparin) tube, or lavender-top (EDTA) tube


If tube other than a gel-barrier tube is used, transfer separated serum or plasma to a plastic transport tube.

Storage Instructions

Room temperature

Stability Requirements



Room temperature

7 days


14 days


14 days

Freeze/thaw cycles

Stable x4

Test Details


This test is used to aid in the diagnosis of primary hyperparathyroidism, hypoparathyroidism, pseudohypoparathyroidism, renal osteodystrophy and vitamin D-resistant rickets.


The 25-(OH) vitamin D form of the hormone is the principle circulating reservoir in plasma and is generally the best indicator of overall vitamin D status. Heterophilic antibodies in human serum can react with reagent immunoglobulins, interfering with in vitro immunoassays. Patients routinely exposed to animals or to animal serum products can be prone to this interference, and anomalous values may be observed.


Immunochemiluminometric assay (ICMA)

Reference Interval

See table.






0 to 6 m



7 m to 1 y



>1 y



Reference Interval developed by in-house study.

Additional Information

Humans get vitamin D from their normal diet, dietary supplements and from exposure to sunlight.1-5 Ultraviolet B irradiation of the skin drives the conversion of 7-dehydrocholesterol to previtamin D3, which is then rapidly converted to vitamin D3.1 Vitamin D from the skin and diet is further metabolized in the liver to 25-(OH) vitamin D (or calcidiol).1-5 Calcidiol is the principle circulating reservoir of vitamin D in plasma and is generally the best indicator of overall vitamin D status. Calcidiol is further converted by the enzyme 25-(OH) D-1α-hydroxylase (CYP27B1) in the proximal tubules of the kidney to the biologically active form of vitamin D, 1,25-(OH)2 vitamin D (or calcitriol).1-5 The renal production of calcitriol is tightly regulated by plasma parathyroid hormone (PTH)1-5 and fibroblast growth factor 23 (FGF-23). FGF-23 is a circulating hormone synthesized by osteocytes and osteoblasts.5-8 Calcitriol and phosphate intake stimulates the synthesis of FGF-23, which, in turn, suppresses calcitriol synthesis and activates calcitriol conversion to inactive metabolites.1-6

Calcitriol is a steroid-like hormone that binds to a specific cytoplasmic vitamin D receptor (VDR) in the cytoplasm of target cells. The calcitriol-VDR complex then migrates into the nucleus, where its effects are mediated at a transcriptional level.5 Renal production of calcitriol is important in the regulation of serum calcium homeostasis and in the maintenance of healthy bone.1,2,9-11 Calcitriol stimulates the absorption of calcium and phosphate by the intestine and increases calcium and phosphate resorption by the kidney.1-6,12,13 Calcitriol also suppresses PTH production and regulates osteoblast function and bone resorption.5 It has been suggested that calcitriol has roles beyond the calcium-skeletal axis.1-5,14

Vitamin D deficiency can affect the production of calcitriol owing to the lack of substrate. A positive correlation between serum levels of calcidiol and calcitriol was observed during seasonal changes. Treatment with calcidiol can normalize calcitriol concentrations in patients with vitamin D deficiency.12,15,16

Calcitriol assessment may be beneficial in patients with chronic kidney failure. Diminished levels of calcitriol can be seen in patients with kidney failure due to reduced 1α-hydroxylase activity and phosphate retention resulting in increased FGF-23 levels.17,18 Impaired calcitriol production plays a major role in the development of secondary hyperparathyroidism as calcitriol deficiency promotes parathyroid gland hyperplasia and increased parathyroid hormone (PTH) synthesis due to the loss of the ability to upregulate vitamin D receptor expression within parathyroid cells.19 This ultimately results in elevated serum PTH and abnormal calcium and phosphorus balance.

Calcitriol measurement may be of use in patients with early-onset rickets or a family history of rickets. Serum calcitriol levels can also be increased in patients with hereditary vitamin D-resistant rickets, a very rare autosomal recessive disorder in which mutations of vitamin D receptor (VDR) impair calcitriol binding to the VDR.20 Patients usually present with hypocalcemia, early-onset rickets, alopecia, and other ectodermal anomalies.20 Other heritable disorders associated with low calcitriol levels include vitamin D–dependent rickets type 1 (inactivating mutation in the 1-hydroxylase gene),21 autosomal-dominant hypophosphatemic rickets (mutation of the gene coding for FGF-23, which prevents its breakdown),22 and X-linked hypophosphatemic rickets (mutations that elevate levels of FGF-23).23 Individuals treated with glucocorticoids or anticonvulsants are at risk of hypocalcemia associated with a low concentration of calcitriol. HIV protease inhibitors have been reported to markedly suppress calcitriol synthesis24,25 In tumor-induced osteomalacia, tumor-secreted FGF-23 inhibits enzyme 1α-hydroxylase and subsequently results in decreased calcitriol synthesis.26

Calcitriol may also be helpful in the diagnosis of parathyroid function disorders. A high serum level of calcitriol, for example, may suggest of primary hyperparathyroidism, whereas a normal or low serum level is more likely found in secondary hyperparathyroidism. Increased calcitriol levels can be seen in some individuals with lymphoproliferative disorders and granulomatous disease including, sarcoidosis, tuberculosis, and inflammatory bowel disease where increased macrophage activity is associated with extrarenal 1α-hydroxylase enzyme activity.27 However, unlike the kidney, the 1α-hydroxylase activity in the macrophages is not controlled by the usual physiologic regulators.14,28


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2. Holick MF, Binkley NC, Bischoff-Ferrare HA, et al. Evaluation, treatment, and prevention of vitamin D deficiency: An Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2011 Jul; 96(7):1911-1930. 21646368
3. Hollis BW. Assessment and interpretation of circulating 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D in the clinical environment. Endocrinol Metab Clin North Am. 2010 Jun; 39(2):271-286. 20511051
4. DeLuca HF. Overview of general physiologic features and functions of vitamin D. Am J Clin Nutr. 2004 Dec; 80(6 Suppl):1689S-1696S. 15585789
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17. Levin A, Bakris GL, Molitch M, et al. Prevalence of abnormal serum vitamin D, PTH, calcium, and phosphorus in patients with chronic kidney disease: Results of the study to evaluate early kidney disease. Kidney International. 2007 Jan; 71(1):31-38. Erratum: 2009 Jun;75(11):1237. 17091124
18. Gutiérrez O, Isakova T, Rhee E, et al. Fibroblast growth factor-23 mitigates hyperphosphatemia but accentuates calcitriol deficiency in chronic kidney disease. J Am Soc Nephrol. 2005 Jul; 16(7):2205-2215. 15917335
19. Llach F, Velasquez Forero F. Secondary hyperparathyroidism in chronic renal failure: Pathogenic and clinical aspects. Am J Kidney Dis 2001 Nov; 38(5 Suppl 5): S20–S33. 11689384
20. Malloy PJ, Feldman D. Genetic disorders and defects in vitamin D action. Endocrinol Metab Clin North Am. 2010 Jun; 39(2):333-346. 20511055
21. Kitanaka S, Takeyama K, Murayama A, Kato S. The molecular basis of vitamin D-dependent rickets type I. Endocr J. 2001 Aug; 48(4):427-432. 11603564
22. White KE, Jonsson KB, Carn G, et al. The autosomal dominant hypophosphatemic rickets (ADHR) gene is a secreted polypeptide over expressed by tumors that cause phosphate wasting. J Clin Endocrinol Metab. 2001 Feb; 86(2):497-500. 11157998
23. Ruppe MD, Brosnan PG, Au KS, Tran PX, Domínguez BW, Northrup H. Mutational analysis of PHEX, FGF23 and DMP1 in a cohort of patients with hypophosphatemic rickets. Clin Endocrinol (Oxf). 2011 Mar; 74(3):312-318. 21050253
24. Cozzolino M, Vidal M, Arcidiacono MV, Tebas P, Yarasheski KE, Dusso AS. HIV-protease inhibitors impair vitamin D bioactivation to 1,25-dihydroxyvitamin D. AIDS. 2003 Mar 7; 17(4):513-520. 12598771
25. Bonjoch A, Figueras M, Estany C, et al. High prevalence of and progression to low bone mineral density in HIV-infected patients: A longitudinal cohort study. AIDS. 2010 Nov 27; 24(18):2827-2833. 21045635
26. Habra MA, Jiménez C, Huang SC, et al. Expression analysis of fibroblast growth factor-23, matrix extracellular phosphoglycoprotein, secreted frizzled-related protein-4, and fibroblast growth factor-7: identification of fibroblast growth factor-23 and matrix extracellular phosphoglycoprotein as major factors involved in tumor-induced osteomalacia. Endocr Pract. 2008 Dec; 14(9):1108-1114. 19158050
27. Inui N, Murayama A, Sasaki S, et al. Correlation between 25-hydroxyvitamin D3 1 alpha-hydroxylase gene expression in alveolar macrophages and the activity of sarcoidosis. Am J Med. 2001 Jun 15; 110(9):687-693. 11403752
28. Overbergh L, Stoffels K, Waer M, Verstuyf A, Bouillon R, Mathieu C. Immune regulation of 25-hydroxyvitamin D-1alpha-hydroxylase in human monocytic THP1 cells: Mechanisms of interferon-gamma-mediated induction. J Clin Endocrinol Metab. 2006 Sep; 91(9):3566-3574. 16787983


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Fournier A, Moriniere P, Boudaillez B, et al. 1,25 (OH) 2 vitamin D3 deficiency and renal osteodystrophy: Should its well-accepted pathogenetic role in secondary hyperparathyroidism lead to its systematic preventive therapeutic use? Nephrol Dial Transplant. 1987; 2(6):498-503 (review). 3126450
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Order Code Order Code Name Order Loinc Result Code Result Code Name UofM Result LOINC
081091 Calcitriol(1,25 di-OH Vit D) 62290-2 081092 Calcitriol(1,25 di-OH Vit D) pg/mL 62290-2

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