The site, parathyroid.com has an excellent explanation of secondary hyperparathyroidism.
- Chronic Kidney Disease that produces 1) Decreased levels of 1,25-dihydroxyvitamin D, 2) Hyperphosphatemia, 3) Hypocalcemia.
- Vitamin D deficiency (due to low dietary intake/lack of sun exposure, malabsorption, liver disease, and other chronic illness)
Related Article: Tertiary Hyperparathyroidism.
Note: To understand how CKD causes decreased levels of 1,25-dihydroxyvitamin D, Hyperphosphatemia, and Hypocalcemia, think of 1) the function of the Parathyroid Hormone. 2) Vitamin D Action.
PTH stimulates good working kidneys to make1,25-Dihydroxyvitamin D3 (Calcitriol). Calcitriol, an errand boy of PTH, joins PTH to reabsorb calcium from the kidneys and excrete phosphate. PTH also invites Calcitriol with it to stimulate osteoclasts in the bone to release calcium. Finally, PTH sends Calcitriol alone to go and tell the intestines to absorb more calcium. All these activities raise serum calcium and lower phosphate. In really advanced CKD, PTH can’t get the kidneys to make Calcitriol or to absorb calcium and secrete phosphate. As such, the parathyroid glands crank up production of PTH since diseased kidneys (in CKD) become resistant to PTH. So PTH rises, calcium is low (or unusually “normal” for the level of PTH), and phosphate rises.
That’s why Chronic kidney disease patients are often on phosphate binders (Sevelamer) and Calcitriol.
Further Reading / Reference
http://www.parathyroid.com/secondary-hyperparathyroidism.htm