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Test ID: PTH2 Parathyroid Hormone, Serum

Reporting Name

Parathyroid Hormone (PTH), S

Useful For

Diagnosis and differential diagnosis of hypercalcemia


Diagnosis of primary, secondary, and tertiary hyperparathyroidism


Diagnosis of hypoparathyroidism


Monitoring end-stage kidney failure patients for possible renal osteodystrophy

Clinical Information

Parathyroid hormone (PTH) is produced and secreted by the parathyroid glands, which are located along the posterior aspect of the thyroid gland. The hormone is synthesized as a 115-amino acid precursor (pre-pro-PTH), cleaved to pro-PTH, and then to the 84-amino acid molecule, PTH (numbering, by universal convention, starting at the amino terminus). The precursor forms generally remain within the parathyroid cells.


Secreted PTH undergoes cleavage and metabolism to form carboxyl-terminal fragments (PTH-C), amino-terminal fragments (PTH-N), and mid-molecule fragments (PTH-M). Only those portions of the molecule that carry the amino terminus (ie, the whole molecule and PTH-N) are biologically active. The active forms have half-lives of approximately 5 minutes. The inactive PTH-C fragments, with half-lives of 24 to 36 hours, make up more than 90% of the total circulating PTH and are primarily cleared by the kidneys. In patients with kidney failure, PTH-C fragments can accumulate to very high levels. PTH 1-84 is also elevated in these patients, with mild elevations being considered a beneficial compensatory response to end organ PTH resistance, which is observed in kidney failure.


The serum calcium level regulates PTH secretion via negative feedback through the parathyroid calcium sensing receptor (CASR). Decreased calcium levels stimulate PTH release. Secreted PTH interacts with its specific type II G-protein receptor, causing rapid increases in renal tubular reabsorption of calcium and decreased phosphorus reabsorption. It also participates in long-term calciostatic functions by enhancing mobilization of calcium from bone and increasing kidney synthesis of 1,25-dihydroxy vitamin D, which, in turn, increases intestinal calcium absorption. In rare inherited syndromes of parathyroid hormone resistance or unresponsiveness, and in kidney failure, PTH release may not increase serum calcium levels.


Hyperparathyroidism causes hypercalcemia, hypophosphatemia, hypercalcuria, and hyperphosphaturia. Long-term consequences are dehydration, kidney stones, hypertension, gastrointestinal disturbances, osteoporosis, and sometimes neuropsychiatric and neuromuscular problems. Hyperparathyroidism is most commonly primary and caused by parathyroid adenomas. It can also be secondary in response to hypocalcemia or hyperphosphatemia. This is most commonly observed in kidney failure. Long-standing secondary hyperparathyroidism can result in tertiary hyperparathyroidism, which represents the secondary development of autonomous parathyroid hypersecretion. Rare cases of mild, benign hyperparathyroidism can be caused by inactivating CASR genetic variants.


Hypoparathyroidism is most commonly secondary to thyroid surgery but can also occur on an autoimmune basis or due to activating CASR genetic variants. The symptoms of hypoparathyroidism are primarily those of hypocalcemia with weakness, tetany, and possible optic nerve atrophy.


Approximately 90% of the patients with primary hyperparathyroidism have elevated parathyroid hormone (PTH) levels. The remaining patients have normal (inappropriate for the elevated calcium level) PTH levels. Approximately 40% of the patients with primary hyperparathyroidism have serum phosphorus levels below 2.5 mg/dL, and about 80% have serum phosphorus levels below 3.0 mg/dL.


A (appropriately) low PTH level and high phosphorus level in a hypercalcemic patient suggests that the hypercalcemia is not caused by PTH or PTH-like substances.


A (appropriately) low PTH level with a low phosphorus level in a patient with hypercalcemia suggests the diagnosis of paraneoplastic hypercalcemia caused by parathyroid-related peptide (PTHRP). PTHRP shares N-terminal homology with PTH and can transactivate the PTH receptor. It can be produced by many different tumor types.


A low or normal PTH in a patient with hypocalcemia suggests hypoparathyroidism, provided the serum magnesium level is normal. Low magnesium levels inhibit PTH release and action and can mimic hypoparathyroidism.


Low serum calcium and high PTH levels in a patient with normal kidney function suggest resistance to PTH action (pseudohypoparathyroidism type 1a, 1b, 1c, or 2) or, very rarely, bio-ineffective PTH.


A limited number of the PTH-C fragments, which accumulate in kidney failure, chiefly PTH 7-84, cross-react in this and other intact PTH assays. PTH 1-84 is also elevated in kidney failure, with mild elevations being considered beneficial. Consequently, when measured with an intact PTH assay, concentrations of 1.5 to 3 times the upper limit of the healthy reference range appear to represent the optimal range for end-stage kidney failure patients. Lower concentrations may be associated with adynamic renal bone disease, while higher levels suggest possible secondary or tertiary hyperparathyroidism, which can result in high-turnover renal osteodystrophy.


Some patients with moderate hypercalcemia and equivocal phosphate levels, who have either mild elevations in PTH or (inappropriately) normal PTH levels, may be suffering from familial hypocalciuric hypercalcemia, which is due to inactivating CASR genetic variants. The molar kidney calcium to creatinine clearance is typically less than 0.01 in these individuals. The condition can be confirmed by CASR gene sequencing; see CASRZ / CASR Gene, Full Gene Analysis, Varies.

Report Available

Same day/1 to 2 days

Day(s) Performed

Monday through Saturday

Clinical Reference

1. Boudou P, Ibrahim F, Cormier C, Chabas A, Sarfati E, Souberbielle JC: Third- or second-generation parathyroid hormone assays: a remaining debate in the diagnosis of primary hyperparathyroidism. J Clin Endocrinol Metab. 2005 Dec;90(12):6370-6372

2. Silverberg SJ, Bilezikian JP: The diagnosis and management of asymptomatic primary hyperparathyroidism. Nat Clin Pract Endocrinol Metab. 2006 Sep;2(9):494-503

3. Brossard JH, Cloutier M, Roy L, Lepage R, Gascon-Barre M, D'Amour P: Accumulation of a non-(1-84) molecular form of parathyroid hormone (PTH) detected by intact PTH assay in renal failure: importance in the interpretation of PTH values. J Clin Endocrinol Metab. 1996 Nov;81(11):3923-3929

4. Garfield N, Karaplis AC: Genetics and animal models of hypoparathyroidism. Trends Endocrinol Metab. 2001 Sep;12(7):288-294

5. Sakhaee K: Is there an optimal parathyroid hormone level in end-stage renal failure: the lower the better? Curr Opin Nephrol Hypertens. 2001 May;10(3):421-427

6. Vetter T, Lohse MJ: Magnesium and the parathyroid. Curr Opin Nephrol Hypertens. 2002 Jul;11(4):403-410

7. Bilezikian JP, Potts JT Jr, Fuleihan GEH, et al: Summary statement from a workshop on asymptomatic primary hyperparathyroidism: a perspective for the 21st century. J Clin Endocrinol Metab. 2002 Dec;87(12):5353-5361

8. Minisola S, Pepe J, Piemonte S, Cipriani C: The diagnosis and management of hypercalcaemia. BMJ. 2015 Jun 2;350:h2723

9. Cooper MS: Disorders of calcium metabolism and parathyroid disease. Best Pract Res Clin Endocrinol Metab. 2011 Dec;25(6):975-983. doi: 10.1016/j.beem.2011.07.001

10. De Sanctis V, Soliman A, Fiscina B: Hypoparathyroidism: from diagnosis to treatment. Curr Opin Endocrinol Diabetes Obes. 2012 Dec;19(6):435-442. doi: 10.1097/MED.0b013e3283591502

Method Name


Specimen Type


Specimen Required

Patient Preparation:

1. For 12 hours before specimen collection do not take multivitamins or dietary supplements containing biotin (vitamin B7), which is commonly found in hair, skin, and nail supplements and multivitamins.

2. Patient should be fasting for 12 hours

Collection Container/Tube:

Preferred: Serum gel

Acceptable: Red top

Submission Container/Tube: Plastic vial

Specimen Volume: 1 mL

Collection Instructions: Centrifuge and aliquot serum into a plastic vial.

Specimen Minimum Volume

0.75 mL

Specimen Stability Information

Specimen Type Temperature Time Special Container
Serum Frozen (preferred) 180 days
  Refrigerated  72 hours
  Ambient  8 hours

Reference Values

<1 month: 7.0-59 pg/mL

4 weeks-11 months: 8.0-61 pg/mL

12 months-10 years: 11-59 pg/mL

11 years-17 years: 15-68 pg/mL

18 years and older: 15-65 pg/mL

Test Classification

This test has been cleared, approved, or is exempt by the US Food and Drug Administration and is used per manufacturer's instructions. Performance characteristics were verified by Mayo Clinic in a manner consistent with CLIA requirements.

CPT Code Information


LOINC Code Information

Test ID Test Order Name Order LOINC Value
PTH2 Parathyroid Hormone (PTH), S 2731-8


Result ID Test Result Name Result LOINC Value
PTH2 Parathyroid Hormone (PTH), S 2731-8


If not ordering electronically, complete, print, and send a Renal Diagnostics Test Request (T830) with the specimen. 

Mayo Clinic Laboratories | Endocrinology Catalog Additional Information: