Homozygous FCGR3A-158F mutation is associated with delayed B-cell depletion following rituximab but with preserved efficacy in a patient with refractory lupus nephri - Université de Bretagne Occidentale Access content directly
Journal Articles Clinical Kidney Journal Year : 2013

Homozygous FCGR3A-158F mutation is associated with delayed B-cell depletion following rituximab but with preserved efficacy in a patient with refractory lupus nephri

Abstract

Rituximab (RTX), an anti-CD20 monoclonal antibody, has shown promising results in a small group of systemic lupus erythematosus (SLE) patients treated for lupus nephritis (LN). However, such observations were not confirmed in the double-blind LUNAR study. Accordingly, the factors associated with the clinical response remain to be characterized. We report the case of a young woman with known LN successfully re-treated with RTX and steroids and homozygous for the low-affinity FCG3RA 158F genotype. Although B-cell depletion was delayed, complete remission with anti-DNA antibody negativity and proteinuria normalization were maintained for 5 years. The implications for disease pathogenesis and clinical monitoring are discussed.

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Immunology
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Dates and versions

hal-00827682 , version 1 (04-02-2016)

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Guillaume Seret, Catherine Hanrotel-Saliou, Boutahar Bendaoud, Yannick Le Meur, Yves Renaudineau. Homozygous FCGR3A-158F mutation is associated with delayed B-cell depletion following rituximab but with preserved efficacy in a patient with refractory lupus nephri. Clinical Kidney Journal, 2013, 6 (1), pp.74-76. ⟨10.1093/ckj/sfs162⟩. ⟨hal-00827682⟩

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UNIV-BREST IMMUNO
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