Response of Homocysteine, Cystathionine, and Methylmalonic Acid to Vitamin Treatment in Dialysis Patients
Open Access
- 1 January 2005
- journal article
- Published by Oxford University Press (OUP) in Clinical Chemistry
- Vol. 51 (1) , 196-201
- https://doi.org/10.1373/clinchem.2004.041210
Abstract
Background: Hyperhomocysteinemia is observed in >80% of hemodialysis patients and is considered a risk factor for cardiovascular disease. Vitamin treatment lowers total homocysteine (tHcy) concentrations in plasma and may therefore reduce the associated risk. Current treatment strategies have not achieved normalization of tHcy in the majority of dialysis patients.Keywords
This publication has 30 references indexed in Scilit:
- Esophagogastroduodenoscopy in chronic hemodialysis patients: 2-year clinical experience in a renal unitClinical Nephrology, 2002
- Hyperhomocysteinemia predicts cardiovascular outcomes in hemodialysis patientsKidney International, 2002
- Relationship between methylmalonic acid and cobalamin in uremiaKidney International, 2000
- Effective correction of hyperhomocysteinemia in hemodialysis patients by intravenous folinic acid and pyridoxine therapyKidney International, 1999
- Elevated Fasting Total Plasma Homocysteine Levels and Cardiovascular Disease Outcomes in Maintenance Dialysis PatientsArteriosclerosis, Thrombosis, and Vascular Biology, 1997
- Hyperhomocysteinemia Confers an Independent Increased Risk of Atherosclerosis in End-Stage Renal Disease and Is Closely Linked to Plasma Folate and Pyridoxine ConcentrationsCirculation, 1996
- The effect of a subnormal vitamin B-6 status on homocysteine metabolism.Journal of Clinical Investigation, 1996
- CobalaminCritical Reviews in Clinical Laboratory Sciences, 1996
- Elevation of 2-methylcitric acid I and II levels in serum, urine, and cerebrospinal fluid of patients with cobalamin deficiencyMetabolism, 1993
- THE METHYL FOLATE TRAP A physiological response in man to prevent methyl group deficiency in kwashiorkor (methionine deficiency) and an explanation for folic-acid-induced exacerbation of subacute combined degeneration in pernicious anaemiaThe Lancet, 1981