Homocysteine and transmethylations in uremia.

A F Perna, D Ingrosso, P Castaldo, P Galletti, N G De Santo

Journal: Kidney international. Supplement 2001;78():S230-3

PMID: 11169016

Free Full Text on Elsevier Science View on PubMed

Abstract

Homocysteine is regarded as a cardiovascular risk factor in both the general population and chronic renal failure patients. Among the mechanisms for homocysteine toxicity, its interference with transmethylation reactions, through its precursor/derivative S-adenosylhomocysteine, plays a multifarious role. In uremia, inhibition of S-adenosylmethionine methyl transfer reactions has been reported by independent investigators, using multiple approaches. This has several possible consequences, which can ultimately affect the patient's relative state of health.

Address: Division of Nephrology and Institute of Biochemistry of Macromolecules, SUN School of Medicine, Naples, Italy.

DOI: 10.1046/j.1523-1755.2001.59780230.x

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MeSH Terms: Acylation, Amino Acids, Cardiovascular Diseases, Homocysteine, Humans, Hyperhomocysteinemia, Methylation, Nitroso Compounds, Oxidation-Reduction, Proteins, Uremia