High calcium levels (hypercalcemia)

Hypercalcemia means there is too much calcium in the blood. It is the most common life-threatening complication of cancer in adults. Hypercalcemia develops in 10% to 20% of adults with cancer, but it rarely develops in children. When it develops in people with cancer, it may be called hypercalcemia of malignancy (HCM).

The body uses calcium in different ways. Calcium forms bones and teeth. It also helps muscles contract and blood clot. Calcium also helps the heart and nervous system work normally.

Calcium levels in the blood

Calcium enters the blood in different ways. The level of calcium in the blood is controlled by hormones and the kidneys.

Calcitriol is a hormone form of vitamin D. It helps the intestines take up calcium from foods and drinks. The intestines then release calcium into the blood.

Parathyroid hormone (PTH) helps control the level of calcium in the blood. When blood calcium levels are low, the parathyroid gland releases PTH. PTH stimulates cells in the bones to break bone down and release calcium into the blood. It also tells the kidneys and intestines to absorb more calcium.

The kidneys help control the amount of calcium in the body. They can remove large amounts of calcium from the blood and pass it into the urine (pee).


Hypercalcemia develops when the bones release too much calcium or the kidneys can't get rid of enough calcium. Certain cancers can cause it, especially advanced stages of the following cancers:

Certain types of immunotherapy and hormonal therapy used to treat some cancers can cause hypercalcemia. Medicines for other health problems can also cause hypercalcemia.


Symptoms of hypercalcemia can vary and may get worse as hypercalcemia progresses.

Symptoms of hypercalcemia include:

  • nausea
  • vomiting
  • loss of appetite
  • constipation
  • fatigue
  • muscle weakness
  • increased thirst
  • having to pee (urinate) more often
  • dark yellow pee (urine)
  • little or no sweating
  • abnormal heartbeat
  • confusion and difficulty thinking clearly
  • problems concentrating
  • lethargy
  • kidney stones
  • bone pain or broken bones
  • coma

Report symptoms to your healthcare team as soon as possible.


Your healthcare team will try to find the cause of the hypercalcemia. This includes a physical exam, assessing your symptoms and a neurological exam.

During a neurological exam, your healthcare team will ask you questions and do tests to check your brain, spinal cord and nerve function. They will also check your mental status and coordination, including how well your muscles, senses and reflexes work.

Your healthcare team will also order:

  • blood chemistry tests
  • urinalysis
  • kidney function tests

Kidney function tests and urinalysis look for certain substances in the blood and urine to determine how well the kidneys are working.

Find out more about the tests and procedures used to diagnose hypercalcemia.

Treating hypercalcemia

Once the cause of hypercalcemia is known, your healthcare team can treat it. This includes treating the underlying cancer to lower calcium levels in the blood. You may also need other treatments for hypercalcemia, including the following:

Replacing fluids

Replacing fluids is the first and most important step in treating hypercalcemia. Extra fluids treat dehydration and improve kidney function. When the kidneys work better, they can remove more calcium from the blood.

You will usually be admitted to the hospital to replace fluids. Your healthcare team may have you drink more fluids or give you fluids through a needle in a vein (intravenous fluids).


Your healthcare team may give you a diuretic, which is a drug that increases how much urine the body makes. Diuretics are given after fluid replacement. They force the fluid through your body to increase urine output and stop the body from reabsorbing calcium back into the blood.

You may also be given medicines that stop the breakdown of bone and lower calcium levels in the blood. These drugs may include:

  • Bisphosphonates – drugs that stop the body from breaking down bone and help strengthen bones.
  • Calcitonin – a hormone that acts on the kidneys. It slows or stops the breakdown of bone and absorption of the calcium released into the blood.
  • Corticosteroids – hormones that reduce swelling and lower the body’s immune response.

Denosumab (Xgeva) is a monoclonal antibody that finds and attaches to RANKL, a substance on the surface of bone cells that breaks down bones. When RANKL is targeted and blocked, bones are not broken down as quickly. Denosumab may be given as a treatment for hypercalcemia when bisphosphonates are no longer working.


If your kidneys fail due to cancer or its treatment, you may need dialysis. Dialysis removes wastes from the blood when the kidneys don’t work properly.

Expert review and references

  • Fojo AT . Metabolic emergencies. DeVita VT Jr, Lawrence TS, & Rosenberg SA. Cancer: Principles & Practice of Oncology. 9th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2011: 146: pp. 2142 - 2152.
  • Health Canada . Regulatory Decision Summary: Xgeva . 2015 : https://www.canada.ca/en/services/health.html.
  • Hemphill RR . Hypercalcemia in emergency medicine. eMedicine.Medscape.com. WebMD LLC; 2013.
  • Kaplan M . Hypercalcemia of malignancy. Kaplan M (Ed.). Understanding and Managing Oncologic Emergencies. 2nd ed. Pittsburgh: Oncology Nursing Society; 2013: 4: pp. 103 - 155.
  • Lewis JL . Hypercalcemia. Beers, M. H., & Berkow, R., (Eds.). Merck Manual for Healthcare Professionals. Rahway, NJ: Merck Research Laboratories; 2013.
  • National Cancer Institute. Hypercalcemia (PDQ®) Patient Version. Bethesda, MD: National Cancer Institute; 2012.
  • Topiwala S . Hypercalcemia. National Cancer Institute & National Library of Medicine. MedlinePlus Medical Encyclopedia. Bethesda, MD: National Cancer Institute & National Library of Medicine; 2012.
  • Yeh HS, Berenson JR . Hypercalcemia. Berger AM, Shuster JL Jr, & Von Roenn JH (eds.). Principles and Practice of Palliative Care and Supportive Oncology. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2013: 35: pp. 472 - 480.

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