Primary glomerulopathy can be classified into seven essential patterns based on histopathological studies. The pathogenesis of membranoproliferative glomerulonephritis (MPGN), and membranous nephropathy (MN), which show glomerular IgG deposition and induce mainly nephrotic syndrome, is not known. To clarify the role of IgG subclass in glomerulonephritis, we compared serum concentrations of IgG subclasses, the ratio of serum IgG subclasses to total IgG (%IgG subclass), and glomerular deposition of IgG subclasses between 7 MPGN patients, 21 MN patients, and 9 lupus nephritis (LN) patients. Serum IgG subclasses and %IgG in all groups were almost within normal range based on the values in Japanese healthy adults. In the MPGN and MN groups, the IgG1 concentration was significant lower than that of the LN group (P < 0.001, P < 0.0001, respectively). The IgG2 concentration in the MPGN group decreased significantly compared with that in the LN group (P < 0.05). The %IgG2 of the LN group decreased significantly compared with that of the MN group (P < 0.05). The %IgG3 of the MPGN group was significantly higher that that of the MN group (P < 0.05). The glomerular immunofluorescent intensity of IgG1 and IgG2 were significantly stronger in the LN group than in the MPGN and MN groups (IgG1, P < 0.001, P < 0.01, respectively; IgG2, P < 0.0001, P < 0.0001, respectively). IgG3 in the MPGN and LN groups deposited significantly compared with that in the MN group (P < 0.0001, P < 0.01, respectively). The intensity of IgG4 in the MN group showed a significant difference compared with that in the MPGN and LN groups (P < 0.0001, P < 0.01, respectively). IgG3 is an important factor in the pathogenesis of primary MPGN, while IgG4 relates to glomerular IgG deposition in MN.
We found four novel mutations in the NCCT gene in seven Japanese patients with GS. Moreover, our study suggests that the distribution of mutations in the NCCT gene in Japanese GS patients potentially differs from that in other populations.
Weanalyzed the clinicopathological features and therapy in 19 patients with kidney disease accompanied by hepatitis C viral infection, including 12 patients with mesangial proliferative glomerulonephritis (including eight with IgA nephropathy), six with membranoproliferative glomerulonephritis (MPGN),and one with membranousnephropathy. Persistent hematuria and/ or proteinuria (10 patients) was the most commonfinding, followed by nephrotic syndrome (8 patients). Cryoglobulinemia was detected in six of 19 patients examined (four of six patients with MPGN).Analysis of hepatitis C virus (HCV)-RNAgenotype in 13 patients revealed that nine of them had type II genotype. All four patients with MPGN, who had serum positive for HCV-RNA, had type II genotype. Five patients were treated with interferon-a (IFN-a) without a demonstrable effect on renal impairment, whereas five of ll patients treated with steroids showed improvement of the renal impairment. During the course of steroid therapy, the serum titer of HCV-RNA decreased in 5 of7 patients. These observations suggest that HCVinfection may be associated with several forms ofglomerulonephritis. Type II HGV-RNA mayhave a strong association with MPGN in Japan. Steroid therapy is not contraindicated in patients with HCV-associated nephropathy if they are resistant to IFN-a treatment.
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