Intravenous Immunoglobulin in the Management of Lupus Nephritis

Scott E. Wenderfer,Trisha Thacker

doi:10.1155/2012/589359

Scott E. Wenderfer, Trisha Thacker

Open Access

https://doi.org/10.1155/2012/589359

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Abstract

The occurrence of nephritis in patients with systemic lupus erythematosus is associated with increased morbidity and mortality. The pathogenesis of lupus nephritis is complex, involving innate and adaptive cellular and humoral immune responses. Autoantibodies in particular have been shown to be critical in the initiation and progression of renal injury, via interactions with both Fc-receptors and complement. One approach in the management of patients with lupus nephritis has been the use of intravenous immunoglobulin. This therapy has shown benefit in the setting of many forms of autoantibody-mediated injury; however, the mechanisms of efficacy are not fully understood. In this paper, the data supporting the use of immunoglobulin therapy in lupus nephritis will be evaluated. In addition, the potential mechanisms of action will be discussed with respect to the known involvement of complement and Fc-receptors in the kidney parenchyma. Results are provocative and warrant additional clinical trials.

Highlights

Intravenous immunoglobulin (IVIg) is a biological agent composed of polyclonal antibodies, derived from the plasma of a large pool of healthy donors [1,2,3,4,5]
Articles excluded (i) IVIg use not discussed (ii) Use limited to animal/in vitro models (iii) Review article (iv) Use in systemic lupus erythematosus (SLE) not discussed (v) Use in SLE limited to non-renal disease (vi) Patients reported in subsequent manuscript (vii) Manuscript not available in English∗
In SLE patients, there is no published data on how long exogenous Ig remains present after administration, and there is a lack of consensus on dosing intervals and the duration of therapy

Summary

Introduction

Intravenous immunoglobulin (IVIg) is a biological agent composed of polyclonal antibodies, derived from the plasma of a large pool of healthy donors [1,2,3,4,5]. It has been primarily used to treat hypogammaglobulinemia but has shown promise in treating autoimmune diseases, inflammatory diseases, and cancer. It is FDA approved for the treatment of idiopathic thrombocytopenic purpura (ITP) and Kawasaki’s vasculitis. The effector functions of autoantibodies are mediated by receptors for constant regions of IgG (FcR) or receptors for complement components that bind to antigen antibody immune complexes. Nonspecific polyclonal Ig can form immune complexes that bind to inhibitory-type Fc-receptors [6] These inhibitory Fc-receptors dampen the effector functions of the activating-type FcR and complement receptors [10,11,12].

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