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