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Homocysteine metabolism in renal disease

Coen van Guldener1, Coen D A Stehouwer

  • 1Department of Internal Medicine, Institute for Cardiovascular Research, Vrije Universiteit Medical Centre, Amsterdam, The Netherlands. c.vanguldener@vumc.nl

Clinical Chemistry and Laboratory Medicine
|December 6, 2003
PubMed

Insights

Elevated homocysteine levels (hyperhomocysteinemia) are common in kidney failure, likely due to reduced clearance, not increased production. The precise location of this impaired clearance in renal failure remains unclear.

Area of Science:

  • Nephrology
  • Cardiovascular Medicine
  • Metabolic Disorders

Background:

  • Hyperhomocysteinemia is a cardiovascular risk factor prevalent in end-stage renal disease (85-100% of patients).
  • The relationship between renal function and plasma homocysteine levels is not fully understood.
  • Hyperhomocysteinemia is not considered a direct cause of renal insufficiency.

Purpose of the Study:

  • To investigate the mechanisms linking renal function to plasma homocysteine levels.
  • To differentiate between impaired homocysteine production and clearance in renal failure.
  • To identify the site of homocysteine metabolism alterations in kidney disease.

Main Methods:

  • Arteriovenous extraction studies to assess kidney homocysteine disposal.
  • Measurement of plasma homocysteine metabolites.
  • Oral homocysteine loading tests to calculate plasma homocysteine elimination.
  • Stable isotope techniques using methionine tracers to study whole-body metabolism.

Main Results:

  • Kidney arteriovenous studies did not reveal significant homocysteine disposal by the kidneys.
  • Whole-body metabolism studies suggest decreased homocysteine clearance is the primary cause of hyperhomocysteinemia in renal failure.
  • The exact site of impaired homocysteine clearance in renal failure remains a subject of debate.

Conclusions:

  • Hyperhomocysteinemia in renal failure is predominantly caused by reduced homocysteine clearance rather than increased production.
  • The kidneys do not appear to be a major site for homocysteine disposal.
  • Further research is needed to pinpoint the exact location of impaired homocysteine clearance in patients with kidney disease.

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