Relationship between levels of advanced glycation end-products (AGE) and activity in erythrocyte complement receptor 1 (E-CR1) in hemodialysis patients

  • YAMADA KAORI
    Devision of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine
  • TANIMOTO MITSUO
    Devision of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine
  • GOHDA TOMOHITO
    Devision of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine
  • OHSAWA ISAO
    Devision of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine
  • HAMADA CHIEKO
    Devision of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine
  • OHI HIROYUKI
    Devision of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine
  • HORIKOSHI SATOSHI
    Devision of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine
  • TOMINO YASUHIKO
    Devision of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine

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Other Title
  • 血液透析患者における赤血球膜レセプター1 (E-CR1) と終末糖化産物advanced glycation end-product (AGE) との関連性
  • ケツエキ トウセキ カンジャ ニ オケル セッケッキュウマク レセプター 1 E CR1 ト シュウマツ トウカ サンブツ advanced glycation end product AGE トノ カンレンセイ

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Abstract

Background : Advanced glycation end product (AGE) may play an important role in the development of diabetic nephropathy and its complications. Levels of AGE in chronic renal failure patients, especially hemodialysis (HD), were significantly higher than those in healthy controls. It has been demonstrated that the erythrocyte complement receptor 1 (E-CR1) plays important roles not only in the regulation of complement activation but also the clearance of immune complexes. E-CR1 activity was decreased in HD patients compared with that in healthy controls. Although the cause of low E-CR1 expression considered to be affected by AGE accumulations, it has not yet been clarified in detail. It is postulated that the low E-CR1 level and high serum pentosidine level may be a risk factor for reduced host defenses. In the present study, we investigated serum pentosidine in diabetic nephropathy and HD patients, and the relationship between serum pentosidine levels and E-CR1 activity in HD patients. Methods : The subjects were 50 HD patients (26 were diabetic, and 24 were non-diabetic patients) and 61 diabetic patients without HD. The levels of serum pentosidine were measured at 0.20,180 and 240 min after HD by enzyme-linked immunosorbent assay (ELISA). Quantitation of E-CR1 was performed using Quantum Simply Cellular (QSC) [Flow Cytometry Standard Corp., Fishers, IN]. Results : The levels of serum pentosidine were increased in diabetic nephrology (stage IV). However, there was no significant difference in the levels of serum pentosidine among diabetic patients without or with nephropathy except for that in those receiving HD. A marked increase in serum pentosidine levels was observed in HD patients. The levels of serum pentosidine did not significantly change during HD in either diabetic or non-diabetic patients. There was a significant inverse correlation between the levels of pentosidine and those of E-CR1 in HD patients (r=-0.236, p<0.05). Conclusion : It appears that high levels of serum pentosidine, one of the AGE, may influence the levels of E-CR1 and affect host defenses.

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