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Metabolic consequences of folate-induced reduction of hyperhomocysteinemia in uremia.

A F Perna, D Ingrosso, N G De Santo, P Galletti, M Brunone and V Zappia
JASN December 1997, 8 (12) 1899-1905;
A F Perna
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D Ingrosso
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N G De Santo
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P Galletti
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M Brunone
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V Zappia
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Abstract

Plasma homocysteine, a well-recognized risk factor for cardiovascular disease, is elevated in uremic patients on hemodialysis. The authors have recently demonstrated that one consequence is the reduction in red cell membrane protein methylation levels, caused by a rise of intracellular adenosylhomocysteine, a potent inhibitor of methyltransferases. Protein methylation is involved in a repair mechanism of damaged membrane proteins, and an impairment in methylation leads to the accumulation of altered proteins. Therapy with folates, cofactors in the transformation of homocysteine to methionine, is effective in lowering plasma homocysteine. This article details a study on the metabolic effects of oral methyltetrahydrofolate, the active form of folic acid, on 14 uremic hemodialysis patients. Two months of therapy led to a significant reduction of plasma homocysteine levels, with a proportional response to pre-folate levels. In five of 13 patients with homocysteine levels above 20 microM, plasma homocysteine level was reduced to less than 15 microM. After treatment, levels of adenosylmethionine, the methyl donor in transmethylations, had significantly increased; levels of adenosylhomocysteine had increased to a smaller extent. Therefore, the ratio between the two compounds, an excellent indicator of the presence and the degree of methylation inhibition, was significantly ameliorated. Methionine plasma levels increased after treatment in all patients and were correlated with posttreatment adenosylmethionine levels. It was concluded that treatment with methyltetrahydrofolate brings the plasma homocysteine concentration back to an "acceptable" level, and the metabolic consequences are in the direction of an increase in the normal flow of transmethylations, as monitored by an increase in the [adenosylmethionine]/[adenosylhomocysteine] ratio.

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Journal of the American Society of Nephrology
Vol. 8, Issue 12
1 Dec 1997
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Metabolic consequences of folate-induced reduction of hyperhomocysteinemia in uremia.
A F Perna, D Ingrosso, N G De Santo, P Galletti, M Brunone, V Zappia
JASN Dec 1997, 8 (12) 1899-1905;

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Metabolic consequences of folate-induced reduction of hyperhomocysteinemia in uremia.
A F Perna, D Ingrosso, N G De Santo, P Galletti, M Brunone, V Zappia
JASN Dec 1997, 8 (12) 1899-1905;
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Cited By...

  • 3-Deazaadenosine Prevents Smooth Muscle Cell Proliferation and Neointima Formation by Interfering With Ras Signaling
  • Reply to Drs. Wagner and Koury
  • Plasma Protein Aspartyl Damage Is Increased in Hemodialysis Patients: Studies on Causes and Consequences
  • Isoprenylcysteine Carboxyl Methyltransferase Activity Modulates Endothelial Cell Apoptosis
  • Elevation in S-Adenosylhomocysteine and DNA Hypomethylation: Potential Epigenetic Mechanism for Homocysteine-Related Pathology
  • 5,10-Methylenetetrahydrofolate reductase genotype determines the plasma homocysteine-lowering effect of supplementation with 5-methyltetrahydrofolate or folic acid in healthy young women
  • Controlled Comparison of L-5-Methyltetrahydrofolate Versus Folic Acid for the Treatment of Hyperhomocysteinemia in Hemodialysis Patients
  • Pharmacokinetics of Once Daily Intraperitoneal Cefazolin in Continuous Ambulatory Peritoneal Dialysis Patients
  • Effect of High Dose Folic Acid Therapy on Hyperhomocysteinemia in Hemodialysis Patients: Results of the Vienna Multicenter Study
  • The C677T Methylenetetrahydrofolate Reductase Gene Mutation in Hemodialysis Patients
  • Effects of High-Dose Folic Acid and Pyridoxine on Plasma and Erythrocyte Sulfur Amino Acids in Hemodialysis Patients
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