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Homocysteine and renal disease
1Department of Internal Medicine, University Hospital and Institute for Cardiovascular Research, Vrije Universiteit, Amsterdam, The Netherlands.
Seminars in Thrombosis and Hemostasis
|September 30, 2000
Summary
Elevated homocysteine (hyperhomocysteinemia) is common in kidney failure and linked to vascular disease. Folic acid can lower homocysteine, but further trials are needed to confirm if this reduces cardiovascular events in renal patients.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Nutritional Biochemistry
Background:
- Hyperhomocysteinemia, elevated homocysteine levels, is prevalent in patients with renal failure.
- The exact cause of hyperhomocysteinemia in renal disease is unknown, but impaired homocysteine elimination and metabolism in the uremic environment are suspected.
- Deficiencies in folate, vitamin B6, or vitamin B12 may contribute to this condition.
Purpose of the Study:
- To review the role of hyperhomocysteinemia as a risk factor for atherothrombotic disease in patients with chronic kidney disease.
- To discuss potential mechanisms underlying hyperhomocysteinemia in renal failure.
- To evaluate the efficacy of homocysteine-lowering therapies in this patient population.
Main Methods:
- Review of case-control and prospective studies investigating the association between homocysteine levels and atherothrombotic disease in renal patients.
- Analysis of proposed pathophysiological mechanisms for hyperhomocysteinemia in renal failure.
- Assessment of the impact of folic acid supplementation on plasma homocysteine concentrations.
Main Results:
- Hyperhomocysteinemia is an independent risk factor for atherothrombotic disease in predialysis and end-stage renal disease patients.
- Folic acid administration (1-15 mg/day) can reduce plasma homocysteine levels in renal patients, but levels often remain above 15 micromol/L.
- The effects of vitamin B12 and vitamin B6 on homocysteine levels in renal failure are not clearly established.
Conclusions:
- Hyperhomocysteinemia is a significant risk factor for vascular complications in patients with kidney disease.
- While folic acid shows some efficacy in reducing homocysteine, it may not normalize levels sufficiently.
- Large-scale intervention trials are necessary to determine if homocysteine-lowering therapies can decrease atherothrombotic events in patients with renal failure.