title: Effects of sevelamer on the progression of vascular calcification in patients on chronic haemodialysis.
abstract: OBJECTIVE
  Vascular calcification is thought to be associated with a high cardiovascular mortality rate in patients with end-stage renal disease. Control of hyperphosphataemia is important for the treatment of the vascular calcification. The aim of the present study was to evaluate the effects of sevelamer hydrochloride on the progression of aortic calcification in haemodialysis (HD) patients.
  
  
  METHODS
  42 HD patients were studied in this study and divided into two groups (sevelamer vs. calcium). Sevelamer was added and titrated up to achieve serum P control for 6 months. The estimations of aortic calcification index (ACI) by abdominal computed tomography scans were performed twice in each patient. We compared the changes in serum calcium, phosphorus, intact parathyroid hormone, and lipids in two groups.
  
  
  RESULTS
  Serum phosphorus levels decreased significantly from 6.7 +/- 0.7 to 6.2 +/- 0.5 mg/dl with no changes in serum intact parathyroid hormone levels in the sevelamer group (p < 0.01), and increased from 6.5 +/- 1.0 to 6.7 +/- 1.1 mg/dl in the calcium group (p < 0.05). Serum calcium levels did not change in the sevelamer group and calcium group. The serum levels of total cholesterol decreased significantly from 158.5 +/- 20.7 to 146.2 +/- 24.1 mg/dl (p = 0.024) and the low-density lipoprotein cholesterol level from 65.3 +/- 14.4 to 54.7 +/- 11.6 mg/dl (p = 0.014) in the sevelamer group. Serum C-reactive protein decreased significantly from 0.14 +/- 0.13 to 0.08 +/- 0.11 mg/dl in the sevelamer group (p = 0.038) and significantly increased (0.18 +/- 0.09 vs. 0.22 +/- 0.12 mg/dl) in the calcium group (p = 0.042). The mean changes in ACI (DeltaACI) were 3.6 +/- 1.5% in the sevelamer group and 8.2 +/- 3.1% in the calcium group.
  
  
  CONCLUSIONS
  Sevelamer allows a better serum phosphorus control compared with calcium-based phosphate binder and suppresses the progression of aortic calcification in HD patients.
authors.affiliation: Department of Medicine, Kidney Center, Tokyo Women's Medical University, Tokyo, Japan.
authors.forename: Takashi
authors.initials: T
authors.lastname: Takei
authors.forename: Shigeru
authors.initials: S
authors.lastname: Otsubo
authors.forename: Keiko
authors.initials: K
authors.lastname: Uchida
authors.forename: Keiko
authors.initials: K
authors.lastname: Matsugami
authors.forename: Tomoko
authors.initials: T
authors.lastname: Mimuro
authors.forename: Takashi
authors.initials: T
authors.lastname: Kabaya
authors.forename: Takashi
authors.initials: T
authors.lastname: Akiba
authors.forename: Kosaku
authors.initials: K
authors.lastname: Nitta
mesh_terms: D000368:Aged; D000704:Analysis of Variance; D001012:Aorta, Abdominal / Q000000981:diagnostic imaging; D001018:Aortic Diseases / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000209:etiology; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D002114:Calcinosis / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000209:etiology; D002118:Calcium / Q000097:blood; D002119:Calcium Carbonate / Q000627:therapeutic use; D002614:Chelating Agents / Q000627:therapeutic use*; D018450:Disease Progression; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood / Q000150:complications* / Q000628:therapy; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D010281:Parathyroid Hormone / Q000097:blood; D010758:Phosphorus / Q000097:blood; D011073:Polyamines / Q000627:therapeutic use*; D006435:Renal Dialysis; D000069603:Sevelamer; D012720:Severity of Illness Index; D018709:Statistics, Nonparametric; D014057:Tomography, X-Ray Computed
chemical_list: D015415:Biomarkers; D002614:Chelating Agents; D008055:Lipids; D010281:Parathyroid Hormone; D011073:Polyamines; D010758:Phosphorus; D002097:C-Reactive Protein; D000069603:Sevelamer; D002119:Calcium Carbonate; D002118:Calcium