Homocysteine and chronic renal failure

Citation
Af. Perna et al., Homocysteine and chronic renal failure, MIN ELECT M, 25(4-6), 1999, pp. 279-285
Citations number
18
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
MINERAL AND ELECTROLYTE METABOLISM
ISSN journal
03780392 → ACNP
Volume
25
Issue
4-6
Year of publication
1999
Pages
279 - 285
Database
ISI
SICI code
0378-0392(199907/12)25:4-6<279:HACRF>2.0.ZU;2-F
Abstract
Homocysteine, a sulfur amino acid, is an important methionine derivative, w hich has been implicated in the pathogenesis of atherothrombosis, Although only observational, epidemiological studies are available at present, the e vidence of an association between hyperhomocysteinemia and increased cardio vascular risk is quite strong and this is confirmed also in a population of chronic renal failure patients. From a biochemical standpoint at least three mechanisms have been so far su mmoned in order to explain homocysteine toxicity including: oxidation, hypo methylation, and acylation. Proteins are believed to play a crucial role as homocysteine molecular targets. Interference with the functions of several of such macromolecules has been so far described being mediated by any of the above mechanisms, Vitamins may positively influence homocysteine metabolism, thus facilitatin g the metabolic clearance of this compound. Therefore they are presently co nsidered as potential means for reducing plasma levels of this amino acid a nd preventing vascular occlusions in hyperhomocysteinemic patients. These c ompounds, with special regard to folate, are eligible for interventional cl inical trials, from which the definitive answer on the role of homocysteine in atherothrombosis is expected. Copyright (C) 2000 S. Karger AG, Basel.