Homocysteine may be a marker, not a cause, of renal trouble, study suggests
TUESDAY, Sept. 11 (HealthDay News) -- Lowering blood levels of an inflammation-linked protein called homocysteine won't help people with serious kidney disease live any longer, new research concludes.
The study, which is published in the Sept. 12 issue of the Journal of the American Medical Association, found that although people who took extra folic acid, vitamin B6 and vitamin B12 were able to significantly lower their homocysteine levels, that change had no effect on their risk of death or heart attack or stroke.
Lowered homocysteine also had no effect on the risk of leg amputations for people with advanced kidney disease or end-stage renal disease.
"We had every expectation at the start of the study that lowering homocysteine would be beneficial," said Dr. Rex L. Jamison, chair and principal investigator for the Homocysteine Study of the Veterans Administration Cooperative Studies Program. "But, our results showed that there was no difference in the number of people who died in the treatment group versus the placebo group, and there was no difference in heart attack, stroke or amputations due to vascular disease," said Jamison, who is professor of medicine at Stanford University School of Medicine.
Numerous studies have linked homocysteine to a variety of bad outcomes, such as heart attack and stroke, leading researchers to believe it might play a role in the development of vascular disease. However, none of the studies has been able to establish a cause-and-effect relationship between homocysteine and disease, leaving open the possibility that high levels of this amino acid might just be a marker of vascular disease, rather than a cause of it.
People with chronic kidney disease or end-stage renal (kidney) disease have much higher levels of homocysteine than the general population, according to the study
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