title: Participation of CR1 (CD35), CR3 (CD11b/CD18) and CR4 (CD11c/CD18) in membranoproliferative glomerulonephritis type I.
abstract: Intraglomerular expression of complement receptors (CR) was investigated chronologically in 22 repeatedly biopsied patients with membranoproliferative glomerulonephritis (MPGN) type I by indirect immunoperoxidase staining using MoAbs. Patients were divided into two groups based on whether intraglomerular C3c deposition was decreased at the second biopsy (2nd Bx) (group A, n = 12), or not (group B, n = 10). At the first biopsy (1st Bx), the severity of glomerular injury and the degree of glomerular C3c deposition were compatible between the two groups. Four patterns of CR1 (CD35) expression on podocytes were recognized: normal; generally decreased; focally/segmentally lost; and completely lost. The numbers of CR3 (CD11b/CD18)- and CR4 (CD11c/CD18)-positive cells per glomerular cross-section were counted. At the 1st Bx, no significant difference was found in the number of CR3+ or CR4+ cells between the two groups. At the 2nd Bx, the numbers of both the CR3+ and CR4+ cells were significantly decreased only in group A (P < 0.01). The numbers of CR3+ and CR4+ cells were significantly higher in cases with moderate or marked C3c deposits than in those with no or mild C3c deposits. The intensity of CR1 expression in group B was less than that in group A at both the 1st and 2nd Bx (1st, P < 0.05; 2nd, P < 0.01), and chronological improvement of CR1 expression was observed only in group A. The severity of glomerular injury was increased only in group B (P < 0.01), and was associated with persistent massive proteinuria and hypocomplementaemia. Our results suggest that, in cases with an adverse outcome, a more severe defect of CR1 initially exists and the expression of CR1 is not recoverable chronologically. This irreversible decrease or loss of CR1 may partly contribute to the continuous C3c deposition and intraglomerular infiltration of CR3+ and CR4+ cells.
authors.affiliation: Second Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
authors.forename: J
authors.initials: J
authors.lastname: Soma
authors.forename: T
authors.initials: T
authors.lastname: Saito
authors.forename: J
authors.initials: J
authors.lastname: Seino
authors.forename: H
authors.initials: H
authors.lastname: Sato
authors.forename: T
authors.initials: T
authors.lastname: Ootaka
authors.forename: A
authors.initials: A
authors.lastname: Yusa
authors.forename: K
authors.initials: K
authors.lastname: Abe
mesh_terms: D000293:Adolescent; D000328:Adult; D018821:CD18 Antigens / Q000276:immunology*; D002648:Child; D005260:Female; D015432:Glomerulonephritis, Membranoproliferative / Q000276:immunology*; D006801:Humans; D007150:Immunohistochemistry; D016167:Integrin alphaXbeta2 / Q000276:immunology*; D016177:Macrophage-1 Antigen / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D017463:Receptors, Complement 3b / Q000276:immunology*; D013997:Time Factors
chemical_list: D018821:CD18 Antigens; D016167:Integrin alphaXbeta2; D016177:Macrophage-1 Antigen; D017463:Receptors, Complement 3b