Vitamin D prohormone in the treatment of secondary hyperparathyroidism in patients with chronic kidney disease

Abstract

Secondary hyperparathyroidism (sHPT) represents the adaptive and very often, finally, maladaptive response of the organism to control the disturbed homeostasis of calcium, phosphorus, and vitamin D metabolism caused by declining renal function in chronic kidney disease (CKD). sHPT leads to cardiovascular and extravascular calcifications and is directly linked to an increased risk of cardiovascular morbidity and mortality as well as excess all-cause mortality. Vitamin D plays an important role in the development of sHPT. CKD patients are characterized by a high prevalence of hypovitaminosis D. Supplementation with both vitamin D prohormones cholecalciferol and ergocalciferol enables the achievement and maintenance of a normal vitamin D status when given in adequate doses over an appropriate treatment period. In patients with earlier stages of CKD, sHPT is influenced by and can be successfully treated with vitamin D prohormone supplementation, whereas in patients with very late stages of CKD and those requiring dialysis, treatment with prohormones seems to be of limited efficacy. This review gives an overview of the pathogenesis of sHPT, summarizes vitamin D metabolism, and discusses the existing literature regarding the role of vitamin D prohormone in the treatment of sHPT in patients with CKD.

Keywords: CKD; CKD-MBD; SHPT; cholecalciferol; dialysis; ergocalciferol.

Figure 1

Pathogenesis of secondary hyperparathyroidism in chronic kidney disease. Notes: Dashed lines indicate counter-regulatory pathways. Abbreviations: CaSR, calcium-sensing receptor; FGF23, fibroblast growth factor 23; FGFR1, fibroblast growth factor receptor 1; GFR, glomerular filtration rate; VDR, vitamin D receptor; (s) Klotho, soluble Klotho; PTH, parathyroid hormone.