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• W2068561628 abstract "Most large observational studies available today establish that moderate hyperhomocysteinemia, either genetically or nutritionally determined, is an independent risk factor for myocardial infarction, stroke, and thromboembolic disease. This is also true for chronic renal failure patients, who exhibit a high prevalence of hyperhomocysteinemia (85–100%), which reaches high plasma concentrations (20–40 µ<i>M</i>, while control values range between 8 and 12 µ^M⁻). After a renal transplant, homocysteine levels decrease, but tend to be higher than normal. The cause of hyperhomocysteinemia in renal failure is still obscure, since recent data have questioned the previous notion that a net homocysteine renal extraction and/or excretion take place in man. No matter the cause of its increase, the sulfur amino acid homocysteine is thought to induce an increment in cardiovascular risk through three basic biochemical mechanisms: (1) homocysteine oxidation, with H₂O₂ generation; (2) hypomethylation through S-adenosylhomocysteine accumulation, and (3) protein acylation by homocysteine thiolactone. The final result is membrane protein damage, endothelial damage, and endothelial cell growth inhibition, among other effects. Hyperhomocysteinemia, in general, is susceptible of therapeutic intervention with the vitamins involved in its metabolism. Depending on the cause, vitamin B₆, vitamin B₁₂, betaine, and/or folic acid can be effectively utilized. Chronic renal failure patients benefit from folic acid in high dosage: 1–2 mg are usually not effective (‘relative folate resistance’), while 5–15 mg reduce homocysteine levels to a ‘normative’ range (<15 µ<i>M</i>) in a substantial group of patients. Good results are also obtained in transplant patients, best with a combination of folic and vitamin B₆. The results of the interventional trials focusing on the possible reduction in cardiovascular risk after homocysteine-lowering therapy, both in the general population and in end-stage renal disease, are expected soon, as well as the genetic and biochemical studies in suitable models, with the aim to clarify the cause-effect link suggested by the numerous observational and basic science studies." @default.
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• W2068561628 date "1999-01-01" @default.
• W2068561628 modified "2023-09-25" @default.
• W2068561628 title "Homocysteine, a New Crucial Element in the Pathogenesis of Uremic Cardiovascular Complications" @default.
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• W2068561628 doi "https://doi.org/10.1159/000057428" @default.
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