How CKD causes SHPT

Learn how chronic kidney disease (CKD) causes imbalances
in your blood that lead to the development of secondary hyperparathyroidism (SHPT)1,2

Male secondary hyperparathyroidism patient watering plants with watering can
Kidney failure leads to imbalances in calcium, phosphate and vitamin D hormone1,2
Kidney icon

Your kidneys help to control the amounts of calcium, phosphate and vitamin D hormone in your blood.1,2

Male secondary hyperparathyroidism patient watering plants with watering can

When you have chronic kidney disease, your kidneys gradually become unable to maintain the right balance of these blood parameters.1,2

Too much calcium is filtered and not enough vitamin D is activated

 

Calcium and vitamin D hormone levels begin to drop1,2

Not enough phosphate is filtered

 

Phosphate level begins to rise1,2

To fix the imbalances, parathyroid
hormone is released1,2
Icon showing parathyroid glands

In order to restore balance, your parathyroid glands (four pea-sized glands located in your neck) release a hormone called parathyroid hormone (PTH).1–3

Female secondary hyperparathyroidism patient writing

Parathyroid hormone makes your bones release calcium.2

Parathyroid hormone also makes your kidneys:2

  • Remove less calcium from your blood
  • Activate more vitamin D
  • Remove more phosphate from your blood

In the early stages of chronic kidney disease, the parathyroid hormone works: the levels of vitamin D hormone, calcium and phosphate are brought back into balance, and your parathyroid glands reduce the amount of parathyroid hormone they release.2

However, as chronic kidney disease progresses, your parathyroid glands are forced to release increasingly abnormal amounts of parathyroid hormone. The excessive release of parathyroid hormone by your parathyroid glands due to chronic kidney disease is known as secondary hyperparathyroidism.2

Female secondary hyperparathyroidism patient writing
References
  1. Cunningham J et al. Clin J Am Soc Nephrol. 2011;6:913–21.
  2. Rodriguez M et al. Am J Renal Physiol. 2005;288:F253–64.
  3. Chai MO et al. J Ren Nurs. 2016;8(2):74–9.
  4. Geng G et al. Osteoporos Int. 2019;30:2019–25.
  5. Xu Y et al. Clin Kidney J. 2021;sfab006.