High Parathyroid Hormone (PTH) Explained
What PTH does to your calcium, phosphate, bone and kidneys, the three classic patterns of hyperparathyroidism, and why it can never be read without a same-day calcium result.
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The Quick Answer
PTH (parathyroid hormone) is made by four small glands sitting behind your thyroid, and its whole job is to keep blood calcium inside a tight range. When calcium drops, the glands release more PTH; when calcium rises, they release less. A high PTH simply means the glands are releasing more hormone than usual, but that can be either a disease of the gland itself or a completely normal, appropriate response to something else pulling calcium down.
PTH is never read on its own. It goes alongside a same-day, albumin-corrected calcium (and ideally a vitamin D level), because the identical PTH number means an entirely different diagnosis depending on whether calcium is high, normal, or low. A lab report that lists PTH with no matching calcium result leaves the question open.
The three broad patterns are: primary hyperparathyroidism (high PTH with high calcium, usually a single benign gland, the most common cause of incidentally found high calcium in Australian general practice), secondary hyperparathyroidism (high PTH with low or normal calcium, most often from vitamin D deficiency or chronic kidney disease, and not a parathyroid disease at all), and tertiary hyperparathyroidism (very high PTH in longstanding kidney disease, once the glands have become autonomous). See the full pattern table below.
Typical Australian Reference Ranges
Exact cut-offs vary between Sonic, Healius, Australian Clinical Labs, Dorevitch, Laverty, QML, Capital Pathology, SA Pathology and PathWest, and between the specific intact PTH assay each lab uses, so always compare your own result to the interval printed on your report rather than the numbers below.
Intact PTH
1.6-6.9 pmol/L
Some labs report roughly 15-65 pg/mL instead. Multiply pmol/L by about 9.4 to approximate pg/mL.
Corrected calcium
2.10-2.60 mmol/L
Corrected for albumin, or measured directly as ionised calcium (1.15-1.30 mmol/L).
Phosphate
0.75-1.50 mmol/L
Usually low in primary hyperparathyroidism, and often high in kidney-related secondary hyperparathyroidism.
Children have their own age-adjusted PTH and calcium ranges, and pregnancy shifts calcium handling substantially, so pregnancy-specific interpretation always needs a GP or obstetrician familiar with the individual case.
How PTH Controls Calcium, Phosphate, Bone and the Kidney
The parathyroid glands carry a calcium-sensing receptor on their surface that constantly monitors blood calcium. When calcium drops even slightly, PTH release increases within minutes and acts on three targets at once to bring it back up.
Bone
PTH stimulates osteoclasts, the cells that break down bone, releasing both calcium and phosphate into the bloodstream. Chronic PTH excess thins bone over years, particularly cortical bone in the forearm.
Kidney
PTH increases calcium reabsorption in the distal kidney tubule (keeping calcium in the body) while reducing phosphate reabsorption (pushing phosphate out in urine). It also switches on the enzyme that activates vitamin D.
Gut (via vitamin D)
The active vitamin D that PTH generates increases calcium and phosphate absorption from food. This is why vitamin D status changes how much PTH is needed to maintain the same calcium level.
Interpreting PTH With Calcium: The Key Patterns
PTH and calcium are read as a pair, because the calcium level is what separates a diseased gland from a healthy gland doing its job. The five patterns below cover almost every high PTH result seen in Australian general practice.
Primary Hyperparathyroidism
Autonomous PTH secretion, independent of the calcium feedback loop that would normally switch the glands off.
Causes: A solitary parathyroid adenoma accounts for 80 to 85% of cases. Multi-gland hyperplasia makes up 10 to 15% (consider MEN1 or MEN2A if the patient is young or several glands are affected). Parathyroid carcinoma is rare, under 1% of cases.
The most common cause of hypercalcaemia found incidentally on a routine blood test in Australian general practice, particularly in postmenopausal women.
Secondary Hyperparathyroidism
An appropriate, compensatory rise in PTH driven by something else pulling calcium down. This is a normal response, not parathyroid disease.
Causes: Vitamin D deficiency is the most common driver seen in Australia. Chronic kidney disease reduces activation of vitamin D and causes phosphate retention. Malabsorption, including coeliac disease, impairs calcium and vitamin D uptake. Bisphosphonate or denosumab therapy pushes calcium into bone, transiently lowering serum calcium and driving PTH up.
Correcting the underlying cause, replacing vitamin D, treating coeliac disease, or reviewing a bone medication usually normalises PTH over weeks to months. Persistent elevation in chronic kidney disease can progress to tertiary hyperparathyroidism.
Tertiary Hyperparathyroidism
Long-standing secondary hyperparathyroidism causes the glands to become autonomous, continuing to secrete large amounts of PTH even after the original stimulus is treated.
Causes: Almost always seen after years of stage 4 to 5 chronic kidney disease or long-term dialysis, and can persist after a kidney transplant.
Managed jointly with a renal physician or endocrinologist, sometimes with a calcimimetic drug such as cinacalcet, or with parathyroid surgery if medical management fails.
Normocalcaemic Primary Hyperparathyroidism
The same underlying parathyroid gland pathology as primary hyperparathyroidism, but the calcium result has not (yet) risen above the normal range.
Causes: Presumed to be an earlier or milder stage of the same adenoma or gland hyperplasia seen in primary hyperparathyroidism.
A diagnosis of exclusion. Vitamin D deficiency, chronic kidney disease and other secondary causes must all be ruled out and corrected first. A minority go on to develop overt hypercalcaemia over several years (around one in five in some follow-up studies, with a wide range between series), so periodic monitoring of calcium and PTH is recommended.
Familial Hypocalciuric Hypercalcaemia (FHH)
A benign, inherited condition that biochemically mimics primary hyperparathyroidism but is not a disease of the parathyroid gland and does not need surgery.
Causes: An autosomal dominant mutation in the calcium-sensing receptor (CASR) gene, usually with a family history of mild, lifelong, symptom-free high calcium.
Distinguished from primary hyperparathyroidism with a 24-hour urine calcium-to-creatinine clearance ratio. A ratio under 0.01 points to FHH; a ratio above 0.02 supports primary hyperparathyroidism. Getting this distinction right matters: operating on someone with FHH fixes nothing, because all four glands are diffusely and mildly overactive rather than one gland being diseased.
Match your own PTH and calcium to one of these patterns
Upload your pathology PDF and SmarterBlood will line up your PTH against your calcium, phosphate and vitamin D automatically, and explain in plain English which of these patterns best fits your result.
Upload Your Blood TestSymptoms: Bones, Stones, Abdominal Groans and Psychic Moans
Bone pain and fragility
Ongoing calcium release out of the skeleton (driven by osteoclast activation) thins cortical bone over time, most noticeably in the forearm. It can cause a dull, deep ache and, eventually, low-trauma fractures.
Kidney stones (flank or groin pain)
Excess calcium filtered into the urine (hypercalciuria) precipitates as calcium oxalate or calcium phosphate stones. Roughly 15 to 20% of people with primary hyperparathyroidism develop at least one kidney stone.
Constipation, nausea and abdominal pain
High calcium slows gut motility and can cause constipation, nausea, loss of appetite and, less commonly, peptic ulcers or pancreatitis when calcium is very high.
Fatigue, low mood and poor concentration
Often described as brain fog. High calcium affects nerve and muscle function broadly, and fatigue or a flat mood are frequently the first things people notice, sometimes years before a diagnosis is made.
Excessive thirst and frequent urination
High calcium interferes with the kidney's ability to concentrate urine, causing polyuria and a compensatory increase in thirst, similar in feel to poorly controlled diabetes.
Muscle weakness and aches
Generalised muscle weakness, most noticeable in the thighs and shoulders when standing from a chair or climbing stairs, is a recognised but often overlooked symptom of high calcium.
Confusion or drowsiness (severe cases)
At very high calcium levels, the nervous system is directly affected and confusion, lethargy or drowsiness can develop. This is a red flag rather than a routine symptom. See the urgent care section below.
No symptoms at all
Most primary hyperparathyroidism in Australia today is found incidentally, on a routine blood test, in someone who feels entirely well. Investigation is still warranted even without symptoms.
High PTH is only one piece of your bone and mineral picture. See how it fits alongside calcium, vitamin D, phosphate and alkaline phosphatase:
Read the Bone Health Markers GuideLonger-Term Consequences If Left Untreated
These consequences relate mainly to sustained high calcium from primary or tertiary hyperparathyroidism. Secondary hyperparathyroidism from a correctable cause generally does not carry the same long-term risks once the underlying deficiency is treated.
Osteoporosis and fragility fractures
Chronic PTH excess drives continuous osteoclast activity, thinning bone (particularly cortical bone in the forearm) faster than it can be rebuilt. This shows up as low bone density on a DEXA scan and raises the risk of low-trauma fractures over years of untreated disease.
Kidney stones (nephrolithiasis)
Persistently high urine calcium promotes stone formation in the kidney and ureter. Stones are one of the two classic reasons (alongside bone loss) that guidelines recommend surgery even in people with only mildly elevated calcium.
Reduced kidney function
Longstanding hypercalcaemia can deposit calcium within kidney tissue itself (nephrocalcinosis) and, over time, gradually reduce eGFR. Kidney function is checked at diagnosis and monitored afterwards for this reason.
Cardiovascular effects
Primary hyperparathyroidism is associated with higher rates of hypertension and vascular calcification, although whether treating the PTH itself reverses this risk is still debated in the research.
Fatigue, low mood and reduced quality of life
Even mild, asymptomatic-appearing primary hyperparathyroidism is associated with measurable reductions in energy, mood and cognitive sharpness on formal testing, many of which improve after successful parathyroidectomy.
When to Seek Urgent Care
Confusion, drowsiness or reduced alertness
Can indicate a hypercalcaemic crisis, generally when corrected calcium rises above roughly 3.5 mmol/L. This needs same-day medical assessment or an emergency department, not a routine GP appointment.
Persistent vomiting or signs of severe dehydration
High calcium impairs the kidney's ability to concentrate urine, and vomiting compounds fluid loss, which further raises calcium in a dangerous cycle. Intravenous fluids are often needed urgently.
Severe flank or groin pain, fever, or inability to pass urine
Suggests an obstructing kidney stone, particularly if accompanied by fever, which can indicate an infected, obstructed kidney requiring urgent urological review.
Severe, new abdominal pain
Very high calcium can trigger acute pancreatitis. Severe, constant upper abdominal pain, especially with vomiting, warrants urgent same-day assessment.
Palpitations, chest pain or an irregular heartbeat with known high calcium
High calcium affects cardiac electrical conduction and can shorten the QT interval or provoke arrhythmias. New cardiac symptoms in this context need urgent review, including an ECG.
What Your GP Will Do Next
Repeat calcium (corrected for albumin) and review your medicines
A single high PTH is never acted on without a same-day, albumin-corrected calcium result. Low albumin falsely lowers total calcium, so the correction formula (or a direct ionised calcium) is used before any pattern is assigned. A medication review happens at the same time, because lithium and thiazide diuretics (such as hydrochlorothiazide or indapamide) can both raise calcium and PTH, and calcium or vitamin D supplements change the picture too.
Check and replace vitamin D, then repeat PTH
Vitamin D deficiency is the single most common driver of a high PTH in Australia. If vitamin D is low, it is replaced first, and PTH is rechecked after several weeks of stable, adequate vitamin D levels before any further conclusions are drawn.
24-hour urine calcium and calcium-to-creatinine clearance ratio
This collection helps rule out familial hypocalciuric hypercalcaemia. A calcium-to-creatinine clearance ratio under 0.01 points toward FHH; a ratio above 0.02 supports primary hyperparathyroidism. It also quantifies how much calcium is spilling into the urine, relevant to kidney stone risk.
Kidney function: eGFR, creatinine and phosphate
Chronic kidney disease is both a common cause of secondary hyperparathyroidism and a consequence of untreated high calcium, so kidney function is checked in every workup. Phosphate is usually low in primary hyperparathyroidism and can be high in kidney-disease-related secondary hyperparathyroidism.
DEXA bone density scan
Assesses the skeletal impact of chronic PTH excess, with particular attention to the distal third of the forearm, a site preferentially affected by parathyroid hormone that is not routinely scanned for other reasons.
Renal tract imaging (ultrasound)
A kidney and bladder ultrasound looks for asymptomatic kidney stones or nephrocalcinosis. Finding stones on imaging, even without symptoms, is one of the recognised criteria for recommending parathyroid surgery.
Sestamibi scan or 4D-CT to localise the gland
Once primary hyperparathyroidism is biochemically confirmed, imaging identifies which of the four parathyroid glands is overactive, allowing a targeted, minimally invasive operation rather than exploring all four glands.
Referral to an endocrine surgeon
Confirmed primary hyperparathyroidism meeting surgical criteria (significant hypercalcaemia, reduced bone density, kidney stones, reduced kidney function, or younger age) is referred for parathyroidectomy, which is curative in the large majority of cases when performed by an experienced endocrine surgeon.
Sources and reference ranges
Adult reference ranges on this page follow the AACB and RCPA harmonised reference intervals unless stated otherwise; the range printed on your own report always takes precedence because laboratories differ.
- healthdirect Australia: thyroid function tests
- Pathology Tests Explained (Australasian Association for Clinical Biochemistry and Laboratory Medicine)
- Australasian Association for Clinical Biochemistry and Laboratory Medicine, publisher of the harmonised reference intervals
- healthdirect Australia: full blood count
High Parathyroid Hormone (PTH): Frequently Asked Questions
What does a high PTH level mean on a blood test?
PTH (parathyroid hormone) is released by four small glands behind the thyroid to keep blood calcium within a tight range. A high PTH means these glands are producing more hormone than usual, either because they have become overactive on their own (primary hyperparathyroidism) or because something else, most often low vitamin D or reduced kidney function, is pulling calcium down and the glands are compensating appropriately (secondary hyperparathyroidism). A high PTH result cannot be interpreted on its own. It must always be read alongside a calcium result taken on the same blood draw, because the same PTH number means a completely different diagnosis depending on whether calcium is high, normal, or low.
What is the difference between primary and secondary hyperparathyroidism?
Primary hyperparathyroidism is a disease of the parathyroid gland itself, usually one gland growing into a benign adenoma and secreting PTH regardless of what the calcium level actually needs. It shows up as high PTH together with high calcium. Secondary hyperparathyroidism is the opposite: the glands are healthy and behaving normally, but they are working overtime because vitamin D deficiency, chronic kidney disease, malabsorption, or a bone medication is lowering calcium and the glands are correctly trying to raise it. It shows up as high PTH with low or normal calcium and is treated by fixing the underlying cause, not by removing the gland.
Can PTH be high with normal calcium?
Yes, and it is one of the trickiest patterns to interpret. Most commonly it reflects secondary hyperparathyroidism from vitamin D deficiency or early kidney disease, and PTH usually falls once the vitamin D is replaced. Less commonly it represents normocalcaemic primary hyperparathyroidism, where the parathyroid gland itself is overactive but the calcium has not yet risen above the normal range. This second diagnosis is only made after vitamin D deficiency, kidney disease, and other secondary causes have been properly excluded and corrected, because treating those first is essential before assuming the parathyroid gland itself is at fault.
What is familial hypocalciuric hypercalcaemia and how is it different from primary hyperparathyroidism?
Familial hypocalciuric hypercalcaemia (FHH) is a benign, inherited condition that biochemically looks almost identical to primary hyperparathyroidism, with a high or high-normal PTH and high calcium. It is caused by a mutation in the calcium-sensing receptor and does not need surgery, because all four glands are mildly and diffusely overactive rather than one gland being diseased. The key test that tells them apart is a 24-hour urine calcium-to-creatinine clearance ratio. A low ratio, generally under 0.01, points to FHH, while a higher ratio supports primary hyperparathyroidism. A family history of mild, lifelong, symptom-free high calcium is another useful clue toward FHH.
What blood and urine tests will my GP order if my PTH is high?
Expect a repeat corrected calcium (adjusted for your albumin level), a vitamin D level, kidney function tests (eGFR and creatinine), and a phosphate level, since PTH normally pushes phosphate down through the kidney. Your GP will also review your medicines, because lithium and thiazide diuretics can raise both calcium and PTH. If vitamin D is low, it is usually replaced first and PTH is rechecked afterwards before anything else is concluded. A 24-hour urine calcium collection, sometimes with a calcium-to-creatinine clearance ratio, helps rule out familial hypocalciuric hypercalcaemia. If primary hyperparathyroidism looks likely, a DEXA bone density scan, a renal ultrasound to check for kidney stones, and imaging of the parathyroid glands themselves (a sestamibi scan or 4D-CT) usually follow.
Does high PTH always mean I need parathyroid surgery?
No. Surgery (parathyroidectomy) is the definitive treatment for confirmed primary hyperparathyroidism causing significant hypercalcaemia, bone loss, or kidney stones, but most people with high PTH do not have this diagnosis. Secondary hyperparathyroidism from vitamin D deficiency or malabsorption is treated by correcting the deficiency, not by operating. Familial hypocalciuric hypercalcaemia does not benefit from surgery at all. Even mild, asymptomatic primary hyperparathyroidism is sometimes managed with monitoring alone in older patients, using periodic calcium, kidney function, and DEXA checks, rather than immediate surgery. Your GP or endocrinologist will weigh your age, calcium level, bone density, and kidney function before recommending an operation.
Can vitamin D deficiency cause high PTH, and will fixing it help?
Yes, vitamin D deficiency is the single most common cause of a high PTH result in Australian general practice. Low vitamin D reduces calcium absorption from the gut, which lowers blood calcium slightly, and the parathyroid glands respond by releasing more PTH to compensate, a completely normal and appropriate reaction called secondary hyperparathyroidism. Replacing vitamin D, which in Australia usually means a daily maintenance supplement and sometimes a higher initial loading dose, corrects the underlying driver, and PTH typically falls back toward the normal range over one to three months. Your GP will usually recheck PTH after vitamin D has been replaced and stable for several weeks, rather than investigating further while vitamin D is still low.
What does "bones, stones, abdominal groans and psychic moans" mean?
This is a long-standing medical mnemonic for the classic symptoms of high calcium caused by primary hyperparathyroidism. "Bones" refers to bone pain and reduced bone density from ongoing calcium release out of the skeleton. "Stones" refers to kidney stones forming from excess calcium in the urine. "Abdominal groans" covers constipation, nausea, abdominal pain and, less commonly, peptic ulcers or pancreatitis. "Psychic moans" refers to fatigue, low mood, poor concentration and, in severe cases, confusion. Many people with mild or early disease have none of these and are picked up only on a routine blood test, which is now the most common way primary hyperparathyroidism is found.
What happens if hyperparathyroidism is left untreated?
Untreated primary hyperparathyroidism causes ongoing loss of calcium from bone, which over years increases the risk of osteoporosis and fragility fractures, particularly in the forearm and hip. Persistently high urine calcium promotes kidney stone formation, and longstanding hypercalcaemia can gradually reduce kidney function through calcium deposits within the kidney tissue itself. There is also a well-documented, if less specific, association with hypertension, vascular calcification, fatigue and depressed mood. Secondary hyperparathyroidism left untreated, most often from unaddressed vitamin D deficiency or advancing kidney disease, can progress over years to tertiary hyperparathyroidism, where the glands become autonomous and much harder to manage medically.
Related Reading
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This page provides general educational information about parathyroid hormone (PTH) and hyperparathyroidism. It is not a substitute for professional medical advice, diagnosis, or treatment. Always consult your GP about abnormal blood test results. Your GP has access to your full medical history and can interpret your results in context. SmarterBlood does not provide medical care.