Related Experiment Videos

Hyperhomocysteinemia in cyclosporine-treated renal transplant recipients

M Arnadottir1, B Hultberg, V Vladov

  • 1Department of Nephrology, University Hospital, Lund, Sweden.

Transplantation
|February 15, 1996
PubMed

Insights

Elevated homocysteine levels are common in kidney transplant recipients, linked to poorer kidney function and potentially exacerbated by cyclosporine. This suggests cyclosporine may interfere with homocysteine metabolism, increasing cardiovascular risk.

Area of Science:

  • Nephrology
  • Cardiovascular Medicine
  • Clinical Chemistry

Background:

  • Moderate hyperhomocysteinemia is an established cardiovascular risk factor.
  • Previous reports indicate elevated homocysteine levels in renal transplant recipients.

Purpose of the Study:

  • To investigate plasma homocysteine concentrations in renal transplant recipients.
  • To compare homocysteine levels between transplant recipients, non-transplanted renal patients, and healthy controls.
  • To explore the influence of cyclosporine and renal function on homocysteine levels.

Main Methods:

  • Plasma total homocysteine concentrations were measured.
  • Glomerular filtration rates (GFR) were assessed.
  • Comparisons were made between renal transplant recipients (n=120), healthy controls (n=60), and non-transplanted renal patients (n=53).
  • Subgroup analyses included recipients with and without cyclosporine treatment.

Main Results:

  • Renal transplant recipients exhibited significantly higher homocysteine levels than healthy controls (19.0 vs. 11.6 mumol/L).
  • Elevated homocysteine was also observed in transplant recipients compared to non-transplanted renal patients (19.0 vs. 16.0 mumol/L).
  • A significant inverse correlation was found between GFR and plasma homocysteine (r = -0.52).
  • Recipients on cyclosporine showed higher homocysteine levels than those not on cyclosporine (19.5 vs. 16.2 mumol/L).
  • Homocysteine levels were higher in recipients with a history of atherosclerotic complications (20.8 vs. 18.5 mumol/L).

Conclusions:

  • Renal insufficiency is a primary driver of hyperhomocysteinemia in non-cyclosporine-treated recipients and non-transplanted renal patients.
  • Cyclosporine appears to contribute to hyperhomocysteinemia through an additional mechanism, possibly interfering with folate metabolism.
  • Elevated homocysteine in transplant recipients may be associated with increased atherosclerotic risk.

Related Concept Videos