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Serological cardiovascular and mortality risk predictors in dialysis patients receiving sevelamer: a prospective

Vincent Matthias Brandenburg1, Georg Schlieper, Nicole Heussen

  • 1Department of Nephrology, University Hospital of the RWTH Aachen, Pauwelsstase 30, Aachen, Germany. vincent.brandenburg@post.rwth-aachen.de

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association
|February 23, 2010
PubMed

Insights

Sevelamer hydrochloride treatment in hemodialysis patients increased serum fetuin-A levels, potentially inhibiting cardiovascular calcification. This effect was delayed but long-lasting, suggesting a novel therapeutic mechanism for chronic kidney disease patients.

Area of Science:

  • Nephrology
  • Cardiovascular Medicine
  • Biochemistry

Background:

  • Patients with chronic kidney disease (CKD) face significantly higher cardiovascular risks.
  • Sevelamer hydrochloride is known to reduce cardiovascular calcification in CKD and end-stage renal disease (ESRD).
  • This study investigates sevelamer's impact on serum fetuin-A and other cardiovascular risk markers in hemodialysis patients.

Purpose of the Study:

  • To assess the effect of sevelamer hydrochloride on serum fetuin-A levels.
  • To evaluate changes in other serological factors related to cardiovascular outcomes and survival.
  • To explore potential anti-calcification mechanisms of sevelamer.

Main Methods:

  • A prospective, three-phase (A-B-A) interventional trial with 57 prevalent hemodialysis patients.
  • Sevelamer was administered during the middle 8-week phase; calcium acetate was used in the other two phases.
  • Analysis of serum biochemistries, including fetuin-A, FGF23, and various uraemic toxins.

Main Results:

  • Serum fetuin-A significantly increased by 21% with sevelamer, with a delayed and long-lasting effect.
  • Significant decreases in total cholesterol, LDL cholesterol, and serum calcium were observed.
  • Albumin, C-reactive protein, and intact parathyroid hormone (iPTH) levels increased, while FGF23 and most uraemic toxins showed no significant change.

Conclusions:

  • Sevelamer treatment in hemodialysis patients leads to a delayed but sustained increase in serum fetuin-A.
  • Elevated fetuin-A may contribute to sevelamer's anti-calcification properties.
  • Further research is needed to elucidate the precise mechanisms linking sevelamer, fetuin-A, and cardiovascular health, as systemic inflammation and uraemic toxin levels did not decrease.
Abstract

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