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[Hyperhomocysteinemia in chronic renal failure.].
E Satta1, A F Perna, C Lombardi
1I Divisione di Nefrologia, II Università degli Studi (SUN), Napoli - Italy.
Summary
Elevated homocysteine (Hcy) in chronic renal failure (CRF) is linked to cardiovascular issues. This review explores Hcy
Area of Science:
- Biochemistry
- Nephrology
- Toxicology
Context:
- Chronic renal failure (CRF) is associated with elevated plasma homocysteine (Hcy) levels.
- Homocysteine is increasingly recognized as a uremic toxin contributing to cardiovascular disease.
- Hyperhomocysteinemia is observed in both the general population and patients with CRF.
Purpose:
- To review the role of homocysteine in chronic renal failure.
- To discuss the mechanisms of homocysteine toxicity in the vasculature.
- To explore the causes of hyperhomocysteinemia in renal decline and potential lowering strategies.
Summary:
- Homocysteine (Hcy), a sulfur amino acid, is a metabolite of methionine and a precursor to S-adenosylhomocysteine (AdoHcy).
- Hcy exhibits toxicity to the endothelium, promotes vascular smooth muscle cell proliferation, enhances platelet aggregation, and affects coagulation and fibrinolysis.
- In CRF, Hcy levels rise due to impaired renal clearance and potential alterations in extrarenal metabolism, leading to consequences like impaired protein methylation and DNA hypomethylation.
Impact:
- Understanding homocysteine's role in CRF is crucial for managing cardiovascular complications.
- Identifying the causes of hyperhomocysteinemia in renal failure may lead to targeted interventions.
- Exploring Hcy-lowering strategies could improve patient outcomes in chronic kidney disease.
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