The CARE study and cardiovascular calcification

Wajeh Y Qunibi1

  • 1Department of Medicine, University of Texas Health Sciences Center, San Antonio 78229-3900, USA. qunibi@uthscsa.edu

Managed Care (Langhorne, Pa.)
|April 12, 2006
PubMed

Insights

Cardiovascular disease (CVD) is a major risk for dialysis patients due to mineral metabolism abnormalities. This review shows calcium acetate effectively manages phosphorus levels without worsening cardiovascular calcification, improving patient longevity.

Area of Science:

  • Nephrology
  • Cardiology
  • Mineral Metabolism

Background:

  • Cardiovascular disease (CVD) causes nearly 50% of deaths in dialysis patients.
  • Abnormalities in mineral metabolism, particularly hyperphosphatemia, contribute significantly to CVD risk.
  • Hyperphosphatemia is common in end-stage renal disease (ESRD) and linked to increased mortality.

Purpose of the Study:

  • To review the role of hyperphosphatemia in CVD pathogenesis in dialysis patients.
  • To evaluate the efficacy and safety of calcium acetate as a phosphate binder.
  • To assess calcium acetate's impact on cardiovascular calcification in the context of K/DOQI guidelines.

Main Methods:

  • Literature review of studies on mineral metabolism, CVD, and phosphate binders in dialysis patients.
  • Analysis of data regarding calcium acetate and sevelamer efficacy and cost-effectiveness.
  • Examination of evidence linking phosphate binders to cardiovascular calcification.

Main Results:

  • Hyperphosphatemia is a critical factor in CVD and mortality risk in dialysis patients.
  • Calcium acetate is a cost-effective phosphate binder compared to sevelamer.
  • Evidence suggests calcium acetate can be used safely, meeting K/DOQI guidelines for elemental calcium, without exacerbating cardiovascular calcification.

Conclusions:

  • Effective management of serum phosphorus and calcium-x-phosphorus product is crucial for improving outcomes in dialysis patients.
  • Calcium acetate presents a viable and cost-effective option for phosphate control.
  • Further research may clarify the precise mechanisms linking mineral metabolism and CVD in ESRD.

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