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Homocysteine targeting of plasma proteins in hemodialysis patients

D W Jacobsen1

  • 1Department of Cell Biology, Lerner Research Institute, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA. jacobsd@ccf.org

Kidney International
|March 7, 2006
PubMed

Insights

Hyperhomocysteinemia is common in kidney disease patients. Folate therapy can normalize protein-N-linked homocysteinylation, a marker linked to cardiovascular disease risk, but not S-linked homocysteinylation.

Area of Science:

  • Nephrology
  • Cardiovascular Disease Research
  • Biochemistry

Background:

  • Hyperhomocysteinemia is a significant, treatable risk factor for cardiovascular disease.
  • Most patients with end-stage renal disease exhibit hyperhomocysteinemia.
  • Protein homocysteinylation contributes to cardiovascular complications in uremia.

Discussion:

  • This study investigates protein-S-linked and protein-N-linked homocysteinylation in hemodialysis patients.
  • The research assesses the impact of folate supplementation on these protein modifications.
  • Distinguishes the effects of folate on different types of protein homocysteinylation.

Key Insights:

  • Protein-N-linked homocysteinylation is significantly reduced by folate therapy in uremic patients.
  • Folate treatment does not normalize protein-S-linked homocysteinylation.
  • This suggests targeted therapeutic strategies for managing cardiovascular risk in renal disease.

Outlook:

  • Further research into the specific mechanisms of S-linked homocysteinylation in uremia.
  • Exploring alternative or adjunctive therapies for normalizing S-linked homocysteinylation.
  • Investigating the long-term cardiovascular outcomes associated with normalized N-linked homocysteinylation.

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