title: Management of secondary hyperparathyroidism in stages 3 and 4 chronic kidney disease.
abstract: OBJECTIVE
  To review approved treatment options for secondary hyperparathyroidism (SHPT) in patients with stages 3 and 4 chronic kidney disease (CKD).
  
  
  METHODS
  Recently published data on the diagnosis and treatment of SHPT in patients with CKD were critically assessed.
  
  
  RESULTS
  Early detection of SHPT is critical for effective treatment. Approximately 40% of patients with stage 3 CKD and 80% of patients with stage 4 have SHPT due to low serum 1,25-dihydroxyvitamin D levels. Appropriate treatment involves suppression of parathyroid hormone (PTH) to normal levels with active vitamin D therapy and phosphate binders. Ergocalciferol or cholecalciferol should be used to correct 25-hydroxyvitamin D levels either before or during active vitamin D therapy. Active vitamin D analogues include calcitriol, doxercalciferol, and paricalcitol. Calcitriol is effective, but has a narrow therapeutic window at higher doses because of hypercalcemia and hyperphosphatemia, which require frequent monitoring. Doxercalciferol is also effective, but has been associated with significant elevations in serum phosphorus requiring greater use of oral phosphate binders. Paricalcitol effectively suppresses PTH with minimal impact on serum calcium and phosphorus. Limited data exist on the use of cinacalcet in treating SHPT in stages 3 and 4 CKD, and it is only approved for use in patients receiving dialysis.
  
  
  CONCLUSIONS
  SHPT is an early and major complication of CKD. Treatment involves suppression of PTH to prevent metabolic bone disease, bone loss, and metabolic complications that may result in marked morbidity and mortality. Early detection of elevated PTH levels with appropriate intervention using active vitamin D therapy, even in the absence of elevated serum phosphorus and reduced serum calcium, is critical.
authors.affiliation: University of Washington School of Medicine, Seattle, Washington, USA. dlandress921@yahoo.com
authors.forename: Dennis L
authors.initials: DL
authors.lastname: Andress
authors.forename: Daniel W
authors.initials: DW
authors.lastname: Coyne
authors.forename: Kamyar
authors.initials: K
authors.lastname: Kalantar-Zadeh
authors.forename: Mark E
authors.initials: ME
authors.lastname: Molitch
authors.forename: Farhad
authors.initials: F
authors.lastname: Zangeneh
authors.forename: Stuart M
authors.initials: SM
authors.lastname: Sprague
mesh_terms: D002117:Calcitriol / Q000627:therapeutic use; D000069449:Cinacalcet; D018450:Disease Progression; D004872:Ergocalciferols / Q000627:therapeutic use; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000097:blood / Q000209:etiology* / Q000628:therapy*; D008954:Models, Biological; D009281:Naphthalenes / Q000627:therapeutic use; D028044:Phosphate-Binding Proteins / Q000097:blood / Q000378:metabolism; D010758:Phosphorus / Q000097:blood / Q000378:metabolism; D011507:Proteinuria / Q000188:drug therapy; D051436:Renal Insufficiency, Chronic / Q000097:blood / Q000150:complications* / Q000473:pathology; D016896:Treatment Outcome; D014808:Vitamin D Deficiency / Q000150:complications / Q000188:drug therapy
chemical_list: D004872:Ergocalciferols; D009281:Naphthalenes; D028044:Phosphate-Binding Proteins; D010758:Phosphorus; C042533:1 alpha-hydroxyergocalciferol; C084656:paricalcitol; D002117:Calcitriol; D000069449:Cinacalcet