title: Acquired loss of erythrocyte complement receptor type 1 in patients with diabetic nephropathy undergoing hemodialysis.
abstract: BACKGROUND
  Complement receptor type 1 on erythrocytes (E-CR1) plays important roles not only in the regulation of complement activation, but also the clearance of immune complexes. Reduced E-CR1 was previously found in patients undergoing hemodialysis (HD). We investigated whether the E-CR1level in HD patients with diabetic nephropathy (DMN) is decreased. The levels of decay accelerating factor (DAF) and CD59 on erythrocytes (E) were also determined to ascertain whether the loss of CR1 is a specific phenomenon or other complement regulatory proteins are also affected.
  
  
  METHODS
  The levels of CR1, DAF, and CD59 on E were analyzed in 176 HD patients with DMN, 101 HD patients with non-diabetes mellitus renal diseases (non-DMN), and 108 healthy individuals. Hind III restriction fragment length polymorphism of intron 27 of the CR1 gene was analyzed. The serum-soluble CR1 levelwas measured by ELISA.
  
  
  RESULTS
  The E-CR1 level was significantly lower in the DMN group than the non-DMN group (p < 0.0001) and healthy individuals (p < 0.05). The E-CR1 level was significantly higher in the non-DMN group than in healthy individuals (p < 0.01). The levels of E-DAF and E-CD59 were significantly lower in the DMN group than non-DMN group (DAF, p < 0.01; CD59, p < 0.0001). Within each genotype of the CR1 gene, the E-CR1 level was significantly lower in the DMN group than in the non-DMN group and healthy individuals (non-DMN, p < 0.01; healthy individuals, p < 0.05). The serum-soluble CR1 level was significantly higher in the DMN group than non-DMN group and control group (p < 0.01 each). However, soluble CR1 did not correlate with E-CR1.
  
  
  CONCLUSIONS
  Acquired loss of E-CR1 was found among HD patients with DMN. From the viewpoint of host defense, it may be a prognostic factor.
authors.affiliation: Division of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan.
authors.forename: Michiro
authors.initials: M
authors.lastname: Wakabayashi
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Ohi
authors.forename: Mariko
authors.initials: M
authors.lastname: Tamano
authors.forename: Kisara
authors.initials: K
authors.lastname: Onda
authors.forename: Teizo
authors.initials: T
authors.lastname: Fujita
authors.forename: Yasuhiko
authors.initials: Y
authors.lastname: Tomino
mesh_terms: D000328:Adult; D000368:Aged; D018958:CD55 Antigens / Q000097:blood; D018957:CD59 Antigens / Q000097:blood; D015247:Deoxyribonuclease HindIII; D003928:Diabetic Nephropathies / Q000097:blood* / Q000628:therapy*; D004912:Erythrocytes / Q000378:metabolism*; D005260:Female; D006801:Humans; D007438:Introns; D008024:Ligands; D008297:Male; D008875:Middle Aged; D012150:Polymorphism, Restriction Fragment Length; D011951:Receptors, Complement / Q000097:blood / Q000172:deficiency* / Q000235:genetics; D006435:Renal Dialysis
chemical_list: D018958:CD55 Antigens; D018957:CD59 Antigens; D008024:Ligands; D011951:Receptors, Complement; D015247:Deoxyribonuclease HindIII