Hyperhomocysteinemia in patients on dialysis, as determined by the methionine loading test.

  • Hirose Satoru
    Fourth Department of Internal Medicine, Saitama Medical Center, Saitama Medical School
  • Kim SongSu
    Fourth Department of Internal Medicine, Saitama Medical Center, Saitama Medical School
  • Matsuda Akihiko
    Fourth Department of Internal Medicine, Saitama Medical Center, Saitama Medical School
  • Itakura Yukihiro
    Fourth Department of Internal Medicine, Saitama Medical Center, Saitama Medical School
  • Mitarai Tetsuya
    Fourth Department of Internal Medicine, Saitama Medical Center, Saitama Medical School
  • Isoda Kazuo
    Fourth Department of Internal Medicine, Saitama Medical Center, Saitama Medical School

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  • 透析患者における高homocysteine血症の検討 methionine負荷試験

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Abstract

It has emerged that hyperhomocysteinemia is one of the risk factors for the development of atherosclerotic vascular disease. Hyperhomocysteinemia has also been observed in patients with end stake renal disease and on dialysis. We used the oral methionine loading test to determine the etiology of the complicating hyperhomocysteinemia in patients on dialysis. Sixteen CAPD patients, 14 HD patients and 15 healthy controls received 0.05g of methionine per kg of body weight after fasting for 12hours. The plasma levels of methionine, cystathionine and cystine were measured by the ninhydrin method, and plasma levels of total homocysteine were determined by the fluoro-HPLC method. CAPD patients exhibited significant increases in plasma total homocysteine, decreases in plasma methionine and increases in plasma cystine. HD patients showed a similar tendency. The methionine loading test revealed retention of plasma methionine, and consecutive increases in plasma homocysteine, cystathionine and cystine in both CAPD and HD patients. These observations suggest that patients on dialysis have specific impairment in the transsulfuration pathway. Considering the decrease in plasma methionine and increase in plasma cystine, patients on dialysis may have an impairment in remethylation from homocysteine to methionine which may play a role in the development of hyperhomocysteinemia.

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