2009
DOI: 10.2215/cjn.06041108
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Successful Treatment of Membranous Glomerulonephritis with Rituximab in Calcineurin Inhibitor-Dependent Patients

Abstract: Conclusions: In patients with MGN with long-term CNI dependence, rituximab can be an effective tool to overcome dependence on CNI, thus avoiding the risk of nephrotoxicity related to the chronic exposure to these drugs.

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Cited by 83 publications
(42 citation statements)
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“…An interesting treatment strategy to overcome dependence of CNI (and thus prevent relapses after drug withdrawal) was proposed by Segarra et al [65] In a study of 13 patients with at least four previous CNI-responsive relapses of nephrotic proteinuria, rituximab treatment (4 weekly doses of 375 mg/m 2 ) enabled CNIs to be successfully withdrawn in all patients. After CNI withdrawal, only three patients suffered from a relapse (19,23, and 28 months after rituximab treatment), all of them were successfully treated with a second course of rituximab.…”
Section: Treatmentmentioning
confidence: 99%
“…An interesting treatment strategy to overcome dependence of CNI (and thus prevent relapses after drug withdrawal) was proposed by Segarra et al [65] In a study of 13 patients with at least four previous CNI-responsive relapses of nephrotic proteinuria, rituximab treatment (4 weekly doses of 375 mg/m 2 ) enabled CNIs to be successfully withdrawn in all patients. After CNI withdrawal, only three patients suffered from a relapse (19,23, and 28 months after rituximab treatment), all of them were successfully treated with a second course of rituximab.…”
Section: Treatmentmentioning
confidence: 99%
“…3,4 Finding that rituximab therapy achieved disease remission and stabilized or even improved renal function in 100 patients at high risk of poor outcomes because of persistent NS pointed to a pathogenic role of antibody-producing lymphocytes in primary MN. 5 Indeed, experimental and human data converge to indicate that deposition along the glomerular basement membrane of immunoglobulins produced by autoreactive B cells initiates the sequence of events, resulting in secondary injury to the glomerular filtering barrier and proteinuria.…”
mentioning
confidence: 99%
“…4 -6 This is in part because of the heterogeneity of disease and lack of reliable biomarkers because of ignorance of the target antigens and nephritogenic antibodies. New strategies to target B-lymphocytes with anti-CD20 antibody [7][8][9] and to inhibit complement 10 have been designed but with varying efficacy. The key to a specific pathophysiology-driven therapy is the understanding of initiating factors leading to the development of immune deposits, which first requires identification of the pathogenic antigens and then the ensuing events mediated by C5b-9.…”
mentioning
confidence: 99%