PARTICIPATION OF CR-1 (CD35), CR3 (CD11B CD18) AND CR4 (CD11C/CD18) IN MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS TYPE-I/

Intraglomerular expression of complement receptors (CR) was investigat ed chronologically in 22 repeatedly biopsied patients with membranopro liferative glomerulonephritis (MPGN) type I by indirect immunoperoxida se staining using MoAbs. Patients were divided into two groups based o n whether intraglomerular C3c deposition was decreased at the second b iopsy (2nd Ex) (group A, n=12), or not (group B, n=10). At the first b iopsy (Ist Ex), the severity of glomerular injury and the degree of gl omerular C3c deposition were compatible between the two groups. Four p atterns of CR1 (CD35) expression on podocytes were recognized: normal; generally decreased; focally/segmentally lost; and completely lost. T he numbers of CR3 (CD11b/CD18)- and CR4 (CD11c/CD18)-positive cells pe r glomerular cross-section were counted. At the Ist Ex, no significant difference was found in the number of CR3(+) or CR4(+) cells between the two groups. At the 2nd Ex, the numbers of both the CR3(+) and CR4( +) cells were significantly decreased only in group A (P<0.01). The nu mbers of CR3(+) and CR4(+) cells were significantly higher in cases wi th moderate or marked C3c deposits than in those with no or mild C3c d eposits. The intensity of CRI expression in group B was less than that in group A at both the Ist and 2nd Ex (Ist, P<0.05; 2nd, P<0.01), and chronological improvement of CRI expression was observed only in grou p A. The severity of glomerular injury was increased only in group B ( P<0.01), and was associated with persistent massive proteinuria and hy pocomplementaemia. Our results suggest that, in cases with an adverse outcome, a more severe defect of CR1 initially exists and the expressi on of CR1 is not recoverable chronologically. This irreversible decrea se or loss of CRI may partly contribute to the continuous C3c depositi on and intraglomerular infiltration of CR3(+) and CR4(+) cells.