Parathyroid Hormone, Intact (PTH)
PTH controls calcium levels in your blood. When calcium drops, PTH rises to bring it back up. When calcium is high, PTH falls. This is why doctors always check PTH and calcium together — the combination reveals whether the problem is in your parathyroid glands, kidneys, or vitamin D levels. High PTH with high calcium usually means a parathyroid problem. High PTH with low calcium often points to vitamin D deficiency or kidney disease.
Parathyroid hormone (PTH) is the master regulator of calcium in your body. Produced by four tiny parathyroid glands located behind your thyroid, PTH continuously monitors blood calcium levels and adjusts them with remarkable precision. When calcium drops even slightly, PTH rises to pull calcium from bones, increase calcium absorption from food, and reduce calcium loss in urine. When calcium is adequate, PTH decreases. This feedback loop keeps calcium in the narrow range essential for nerve function, muscle contraction, and heart rhythm.
Why does this matter? Abnormal PTH levels indicate problems with calcium regulation that can significantly impact health. High PTH (hyperparathyroidism) causes elevated calcium, leading to kidney stones, bone loss, fatigue, and cognitive symptoms. Low PTH (hypoparathyroidism) causes low calcium with muscle cramps, numbness, and potentially dangerous cardiac effects. PTH testing is essential for evaluating abnormal calcium levels, diagnosing parathyroid disorders, monitoring kidney disease, and assessing unexplained bone loss.
Key Benefits of Testing
PTH testing clarifies the cause of abnormal calcium levels. When calcium is high, PTH distinguishes parathyroid-driven causes (PTH elevated or inappropriately normal) from other causes like cancer (PTH suppressed). When calcium is low, PTH shows whether the parathyroid glands are responding appropriately (PTH high) or are the problem (PTH low or inappropriately normal).
In chronic kidney disease, PTH monitoring is essential because failing kidneys disrupt calcium-phosphorus balance, leading to secondary hyperparathyroidism that damages bones and blood vessels. Regular PTH testing guides treatment to prevent these complications.
What Does This Test Measure?
The intact PTH test measures the complete, biologically active parathyroid hormone molecule (84 amino acids). This is the standard PTH assay used clinically. Older assays measured PTH fragments that could give misleading results, particularly in kidney disease. Modern intact PTH assays provide accurate assessment of parathyroid function.
What PTH Does
PTH raises blood calcium through three mechanisms working together. First, it stimulates osteoclasts to break down bone, releasing calcium and phosphorus into blood. Second, it acts on the kidneys to increase calcium reabsorption (keeping calcium in blood rather than losing it in urine) while increasing phosphorus excretion. Third, it stimulates the kidneys to produce active vitamin D (calcitriol), which increases calcium absorption from the intestines.
The parathyroid glands sense blood calcium levels directly through calcium-sensing receptors. When calcium falls, these receptors trigger increased PTH secretion within seconds to minutes. When calcium rises, PTH secretion is suppressed. This tight feedback loop normally maintains calcium within a very narrow range.
PTH and Vitamin D Relationship
PTH and vitamin D work together in calcium regulation, and their relationship is clinically important. PTH stimulates conversion of inactive vitamin D to active calcitriol in the kidneys. In turn, adequate vitamin D helps suppress PTH by improving calcium absorption. When vitamin D is deficient, calcium absorption falls, triggering compensatory PTH elevation (secondary hyperparathyroidism). This is why vitamin D status should be assessed alongside PTH in most clinical situations.
PTH and Phosphorus
PTH also regulates phosphorus, generally moving it opposite to calcium. PTH causes the kidneys to excrete more phosphorus, lowering blood levels. In primary hyperparathyroidism, phosphorus is typically low-normal or low. In kidney disease, inability to excrete phosphorus leads to elevated phosphorus, which further stimulates PTH secretion.
Why This Test Matters
Diagnoses Primary Hyperparathyroidism
Primary hyperparathyroidism occurs when one or more parathyroid glands produce excess PTH, usually due to a benign tumor (adenoma). This is a common condition, affecting about 1 in 500 people, particularly postmenopausal women. The hallmark finding is elevated calcium with elevated or inappropriately normal PTH. Without PTH measurement, the diagnosis cannot be confirmed.
Evaluates Hypocalcemia
When calcium is low, PTH helps determine why. Appropriately elevated PTH indicates the parathyroids are responding normally to low calcium — the problem lies elsewhere (vitamin D deficiency, kidney disease, malabsorption). Low or normal PTH with low calcium indicates hypoparathyroidism — the parathyroid glands themselves are failing, often after thyroid surgery or due to autoimmune destruction.
Essential in Chronic Kidney Disease
As kidney function declines, the kidneys can’t excrete phosphorus or produce active vitamin D effectively. Rising phosphorus and falling vitamin D trigger progressive PTH elevation — secondary hyperparathyroidism. Left untreated, this causes renal osteodystrophy (bone disease) and accelerates cardiovascular calcification. Guidelines recommend regular PTH monitoring starting at CKD stage 3, with treatment to maintain PTH within target ranges.
Investigates Bone Loss
Unexplained osteoporosis or bone loss warrants PTH testing. Subtle primary hyperparathyroidism can cause significant bone loss before calcium becomes obviously elevated. PTH measurement can identify this treatable cause of osteoporosis.
Value of Baseline and Monitoring
For individuals with known parathyroid disorders or kidney disease, regular PTH monitoring tracks disease progression and treatment response. Even in healthy individuals, knowing your baseline PTH alongside calcium provides context for future interpretation if problems develop.
What Can Affect PTH Levels?
Causes of Elevated PTH
Primary hyperparathyroidism — the parathyroid glands overproduce PTH independent of calcium levels:
- Single adenoma (85% of cases) — benign tumor of one gland
- Four-gland hyperplasia (10-15%) — all glands enlarged
- Parathyroid carcinoma (rare, <1%)
- Multiple endocrine neoplasia syndromes (MEN1, MEN2A)
Secondary hyperparathyroidism — PTH rises appropriately in response to low calcium or other stimuli:
- Vitamin D deficiency — very common cause
- Chronic kidney disease — can’t excrete phosphorus or make active vitamin D
- Calcium malabsorption (celiac disease, gastric bypass)
- Inadequate dietary calcium
Tertiary hyperparathyroidism — prolonged secondary hyperparathyroidism (usually from kidney disease) causes autonomous PTH secretion that persists even after kidney transplant.
Causes of Low PTH
Hypoparathyroidism — the parathyroid glands fail to produce adequate PTH:
- Post-surgical — most common cause; parathyroids damaged or removed during thyroid surgery
- Autoimmune — antibodies destroy parathyroid tissue
- Genetic — DiGeorge syndrome, familial isolated hypoparathyroidism
- Infiltrative diseases — hemochromatosis, Wilson disease, metastatic cancer
- Magnesium deficiency — impairs PTH secretion and action
PTH suppression — glands are intact but appropriately suppressed:
- Hypercalcemia from non-parathyroid causes (malignancy, vitamin D toxicity, granulomatous diseases)
Normal Variations
PTH has a circadian rhythm with highest levels in early morning and lowest in afternoon. Levels increase with age. PTH is slightly higher during pregnancy. Significant individual variation exists in baseline PTH levels.
When Should You Get Tested?
Abnormal calcium levels: PTH is essential for interpreting both high and low calcium. Any calcium abnormality should prompt PTH measurement.
Symptoms suggesting calcium imbalance: Fatigue, weakness, depression, cognitive difficulties, kidney stones, bone pain, or fractures (possible hyperparathyroidism). Muscle cramps, numbness, tingling, or spasms (possible hypocalcemia).
Osteoporosis evaluation: Unexplained bone loss or osteoporosis, especially if other causes have been excluded. PTH identifies treatable parathyroid disease.
Chronic kidney disease: Regular monitoring starting at CKD stage 3. Frequency increases as kidney function worsens.
Post-thyroid surgery: Hypoparathyroidism is a potential complication. PTH and calcium should be monitored.
Vitamin D deficiency evaluation: Checking PTH alongside vitamin D determines if deficiency is causing secondary hyperparathyroidism.
Understanding Your Results
PTH results must always be interpreted alongside calcium levels — the two measurements are inseparable clinically. The pattern of PTH and calcium together determines the diagnosis.
High PTH + High calcium = Primary hyperparathyroidism. The parathyroid glands are overproducing PTH despite adequate or high calcium. Evaluation for adenoma and surgical consideration follows.
High PTH + Low calcium = Secondary hyperparathyroidism. PTH is appropriately elevated trying to correct low calcium. Look for vitamin D deficiency, kidney disease, or malabsorption as the underlying cause.
High PTH + Normal calcium = Either early/mild primary hyperparathyroidism (normocalcemic variant) or secondary hyperparathyroidism with successful compensation. Vitamin D status and clinical context guide interpretation.
Low PTH + Low calcium = Hypoparathyroidism. The parathyroid glands are failing. Evaluate for post-surgical, autoimmune, or other causes.
Low PTH + High calcium = Non-parathyroid hypercalcemia. PTH is appropriately suppressed. Consider malignancy (PTHrP-mediated or bone metastases), vitamin D toxicity, or granulomatous disease.
What to Do About Abnormal Results
For Elevated PTH
With high calcium (primary hyperparathyroidism): Confirm with repeat testing. Measure 24-hour urine calcium to exclude familial hypocalciuric hypercalcemia (FHH), a benign mimic. Imaging (neck ultrasound, sestamibi scan) localizes adenoma if surgery planned. Surgery (parathyroidectomy) is curative for most cases and recommended for patients meeting criteria (significant hypercalcemia, kidney stones, osteoporosis, or age <50).
With low/normal calcium (secondary hyperparathyroidism): Identify and treat the underlying cause. Check and replete vitamin D — this alone often normalizes PTH. Evaluate kidney function. Address calcium and vitamin D intake. In CKD, follow nephrology guidelines for phosphorus control and vitamin D supplementation.
For Low PTH
With low calcium (hypoparathyroidism): Calcium and vitamin D supplementation are the mainstays of treatment. Check magnesium and replete if low. Synthetic PTH (Natpara) is available for difficult-to-control cases. Monitor to maintain calcium in low-normal range while avoiding hypercalciuria.
With high calcium: Investigate for malignancy (PTHrP, bone scan), vitamin D toxicity, or granulomatous disease. The suppressed PTH indicates the cause is outside the parathyroid glands.
Related Health Conditions
Primary Hyperparathyroidism
One or more parathyroid glands overproduce PTH, usually due to a benign adenoma. This raises calcium, causing kidney stones, osteoporosis, fatigue, cognitive symptoms, and other manifestations. Diagnosis requires elevated calcium with elevated or inappropriately normal PTH. Surgery is curative for most cases. Learn more →
Hypoparathyroidism
Inadequate PTH production causes low calcium, leading to muscle cramps, numbness, tingling, and potentially seizures or cardiac arrhythmias. Most cases follow thyroid or parathyroid surgery. Treatment requires lifelong calcium and vitamin D supplementation to maintain calcium levels. Learn more →
Chronic Kidney Disease
Failing kidneys disrupt calcium-phosphorus-PTH balance, causing secondary hyperparathyroidism that worsens as CKD progresses. This leads to bone disease (renal osteodystrophy), fractures, and vascular calcification. Managing PTH is a key part of CKD care to prevent these complications. Learn more →
Vitamin D Deficiency
Low vitamin D reduces calcium absorption, triggering compensatory PTH elevation (secondary hyperparathyroidism). Over time, this can weaken bones as PTH mobilizes calcium from the skeleton. Checking PTH alongside vitamin D shows whether deficiency is causing parathyroid activation. Vitamin D repletion typically normalizes PTH. Learn more →
Osteoporosis
Hyperparathyroidism is an important secondary cause of osteoporosis. Chronically elevated PTH causes bone loss, particularly affecting cortical bone. Testing PTH in osteoporosis patients identifies this treatable cause — surgical cure of hyperparathyroidism improves bone density. Learn more →
Kidney Stones
Primary hyperparathyroidism significantly increases kidney stone risk through elevated calcium excretion in urine (hypercalciuria). Up to 20% of hyperparathyroidism patients develop stones. Testing PTH is part of metabolic stone workup, especially for calcium stones. Treating hyperparathyroidism reduces stone recurrence. Learn more →
Hypercalcemia of Malignancy
Cancer can cause high calcium through several mechanisms, most commonly PTHrP (PTH-related peptide) production by tumors or bone metastases releasing calcium. In contrast to hyperparathyroidism, PTH is suppressed (low) because the parathyroids respond appropriately to high calcium. This PTH pattern helps distinguish malignancy from parathyroid disease. Learn more →
Related Biomarkers Often Tested Together
Calcium — Essential companion to PTH; they must be interpreted together.
Vitamin D (25-OH) — Affects PTH levels; deficiency causes secondary hyperparathyroidism.
Phosphorus — Inversely related to PTH; helps characterize parathyroid disorders.
Creatinine/eGFR — Kidney function affects PTH; essential in interpretation.
Magnesium — Low magnesium impairs PTH secretion and can cause hypocalcemia.
Alkaline Phosphatase — Bone turnover marker; often elevated in hyperparathyroidism.
Note: Information provided in this article is for educational purposes and doesn’t replace personalized medical advice.
Frequently Asked Questions
Parathyroid hormone (PTH) is produced by four small parathyroid glands behind your thyroid. It regulates calcium by affecting bones (releasing calcium), kidneys (retaining calcium, excreting phosphorus), and intestines (via vitamin D activation). PTH keeps blood calcium in the precise range needed for normal body function.
PTH and calcium are in a feedback loop — the meaning of one depends entirely on the other. High PTH with high calcium means something very different from high PTH with low calcium. Testing PTH alone without calcium (or vice versa) doesn’t allow proper interpretation.
Hyperparathyroidism means excessive PTH production. Primary hyperparathyroidism is caused by a parathyroid tumor producing too much PTH regardless of calcium level. Secondary hyperparathyroidism is appropriate PTH elevation in response to low calcium or vitamin D. The distinction determines treatment.
Hypoparathyroidism (inadequate PTH production) most commonly follows thyroid surgery when parathyroids are damaged or removed. It also occurs with autoimmune destruction, genetic conditions, or magnesium deficiency. Symptoms result from low calcium: cramps, numbness, tingling.
Failing kidneys can’t excrete phosphorus or produce active vitamin D, leading to low calcium and high phosphorus — both stimulate PTH. This secondary hyperparathyroidism is nearly universal in advanced CKD and causes bone disease and vascular problems if untreated.
Yes — vitamin D deficiency is a very common cause of elevated PTH (secondary hyperparathyroidism). Checking both determines whether vitamin D repletion might normalize PTH, avoiding misdiagnosis of primary hyperparathyroidism.
Fasting is not required, but timing matters. PTH has a circadian rhythm — levels are highest in early morning. For consistency in monitoring, testing at the same time of day is helpful.
References
Key Sources:
- Bilezikian JP, et al. Guidelines for the Management of Asymptomatic Primary Hyperparathyroidism. J Clin Endocrinol Metab. 2014;99(10):3561-3569.
- KDIGO CKD-MBD Update Work Group. KDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of CKD-MBD. Kidney Int Suppl. 2017;7(1):1-59.
- Shoback D. Hypoparathyroidism. N Engl J Med. 2008;359(4):391-403.
