Secondary Hyperparathyroidism in End-Stage Renal Disease: No Longer a Matter for Surgeons?

Blood Purif. 2016;42(1):44-8. doi: 10.1159/000445204. Epub 2016 Apr 2.

Abstract

Hyperphosphatemia, hypocalcemia and vitamin D deficiency are the main factors involved in the pathogenesis of secondary hyperparathyroidism (SHPT). Moreover, the skeletal resistance to parathyroid hormone is not only a high-turnover bone accompanying SHPT, but may also play a crucial role in the onset of low-turnover bone disease in uremia. However, a growing body of evidence suggests that other hormones play a key role in this disease, such as fibroblast growth factor 23, Klotho and sclerostin. SHPT causes both bone-associated and non-skeletal consequences, including cardiovascular calcifications. Furthermore, vitamin D and calcium (Ca)-containing phosphate binders may increase Ca load. Anyway, the rate of parathyroidectomy in end-stage renal disease has greatly decreased during the last decade. Is there any room left for surgeons?

Publication types

  • Review

MeSH terms

  • Hormones / therapeutic use
  • Humans
  • Hyperparathyroidism, Secondary / complications
  • Hyperparathyroidism, Secondary / drug therapy
  • Hyperparathyroidism, Secondary / prevention & control
  • Hyperparathyroidism, Secondary / surgery*
  • Kidney Failure, Chronic / complications*
  • Parathyroidectomy / statistics & numerical data*

Substances

  • Hormones