The Skinny on Secondary Hyperparathyroidism

If you’ve ever helped take care of a patient with chronic kidney disease, you’ve probably noticed that there is always a discussion about the patient’s calcium and phosphorus levels. Take a closer look in the chart and you’ll see that someone has probably checked the patient’s parathyroid hormone (PTH) levels in the past. To understand why chronic kidney disease, calcium, phosphorus, and PTH are all related, let’s dive into the basics of secondary hyperparathyroidism.  

Chronic kidney disease causes serum calcium to be low or low-normal through multiple mechanisms.

The vitamin D (25-OH vitamin D) we get from our diet and skin needs to be processed by the liver and kidneys before it becomes active vitamin D (1,25-OH vitamin D). This active form is then used in the gastrointestinal tract to absorb calcium from food. In chronic kidney disease, this conversion cannot take place, so patients have an active vitamin D deficiency in addition to a 25-OH vitamin D deficiency.

Additionally, diminished kidney function leads to decreased phosphorus clearance. When phosphorus levels in the blood are high, osteoblasts produce FGF-23, which is supposed to help the kidneys clear phosphorus. Unfortunately, FGF-23 also inhibits the conversion of vitamin D into its active form, so patients become even more vitamin D deficient.

Before we continue, let’s summarize with this graphic:

Vitamin D Metabolism in CKD

Low calcium levels stimulate parathyroid glands to kick into overdrive to produce more PTH. PTH usually works to increase serum calcium by increasing calcium absorption in the distal nephron and increasing calcium release from bones via osteoclasts3. However, the distal nephron does not work well in CKD, and over time the skeletal system will develop resistance to high levels of PTH. Both of the mechanisms of PTH are ineffective in this situation.

Post by
Jennifer Kaplan
Sayna Norouzi, MD
Baylor, College of Medicine, Houston, TX


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