title: Calcium salts in the treatment of hyperphosphatemia in hemodialysis patients.
abstract: OBJECTIVE
  Hyperphosphatemia in patients with end-stage renal disease leads to secondary hyperparathyroidism and renal osteodystrophy, and is independently associated with mortality risk. How hyperphosphatemia increases mortality risk is unknown but it may promote cardiovascular calcification. It is recommended that dialysis patients be treated to maintain normal serum phosphorus. Although calcium-based phosphate binders are cost-effective, their long-term safety has been questioned because of their postulated role in progression of cardiovascular calcification. In this regard, sevelamer hydrochloride has been recommended as an alternative phosphate binder. In this review, we will examine these issues and provide rational guidelines for the use of calcium-based phosphate binders.
  
  
  RESULTS
  Results from the calcium acetate Renagel evaluation study indicate that calcium acetate is more effective than sevelamer in controlling serum phosphorus and calcium x phosphorus product in hemodialysis patients. However, in the Treat-to-Goal study dialysis patients treated with sevelamer had less progression of coronary and aortic calcification than patients treated with calcium-containing binders. The mechanism underlying the slower rate of progression of cardiovascular calcification in sevelamer-treated patients remains uncertain but may relate to decreased calcium loading or to dramatic reductions in LDL cholesterol.
  
  
  CONCLUSIONS
  At present, evidence incriminating calcium-containing phosphate binders in the progression of cardiovascular calcification in end-stage renal disease remains largely circumstantial. As calcium acetate is more efficacious and cost-effective than sevelamer, it remains an accepted first-line drug. Treatment with sevelamer hydrochloride should be considered for patients with persistent hypercalcemia during calcium-based binder therapy despite appropriate adjustment of vitamin D therapy.
authors.affiliation: University of Texas Health Sciences Center, San Antonio, Texas, USA. nolan@uthscas.edu
authors.forename: Charles R
authors.initials: CR
authors.lastname: Nolan
authors.forename: Wajeh Y
authors.initials: WY
authors.lastname: Qunibi
mesh_terms: D000085:Acetates / Q000627:therapeutic use; D017610:Calcium Compounds / Q000627:therapeutic use*; D002318:Cardiovascular Diseases / Q000209:etiology; D002986:Clinical Trials as Topic; D004341:Drug Evaluation; D004852:Epoxy Compounds / Q000627:therapeutic use; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000097:blood / Q000188:drug therapy* / Q000209:etiology* / Q000517:prevention & control; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000628:therapy; D028044:Phosphate-Binding Proteins / Q000627:therapeutic use*; D010710:Phosphates / Q000097:blood*; D010758:Phosphorus / Q000097:blood; D011073:Polyamines; D011095:Polyethylenes / Q000627:therapeutic use; D006435:Renal Dialysis / Q000009:adverse effects*; D000069603:Sevelamer; D016896:Treatment Outcome
chemical_list: D000085:Acetates; D017610:Calcium Compounds; D004852:Epoxy Compounds; D028044:Phosphate-Binding Proteins; D010710:Phosphates; D011073:Polyamines; D011095:Polyethylenes; D010758:Phosphorus; D000069603:Sevelamer; C120662:calcium acetate