For citation purposes: Medrano AS, Jaller KR. The current evidence supporting rituximab treatment in primary glomerular diseases causing nephrotic syndrome: Critical review. OA Nephrology 2013 Apr 01;1(1):3.

Critical review

 
Treatment

The current evidence supporting rituximab treatment in primary glomerular diseases causing nephrotic syndrome: Critical review

A Segarra Medrano, K Romero Jaller
 

Authors affiliations

Servicio de Nefrologia, Hospital Vall d’Hebron, Barcelona, Spain

* Corresponding author Email: alsegarr@gmail.com

Abstract

Introduction

Rituximab is a chimeric monoclonal antibody directed against the CD20 receptor on B cells present along all maturational stages of its cycle but not in plasma cells. The administration of one dose of 375 mg/m2 per week for 4 weeks or the administration of a total dose 2 g within a 2-week interval causes depletion of circulating B lymphocytes, which lasts for 6–7 months. Although rituximab was designed for the treatment of relapsing or refractory non-Hodgkin lymphoma B, since its introduction in the therapeutic scene, it was considered an attractive drug for the treatment of various autoimmune diseases mediated by antibodies. The aim of this critical review was to assess the evidence supporting rituximab treatment in primary glomerular diseases causing nephrotic syndrome.

Conclusion

Current evidence from observational studies suggests that rituximab can induce the remission of nephrotic syndrome in patients suffering from membranous glomerulonephritis, minimal change nephropathy and focal segmental glomerulosclerosis. However, there is an absence of controlled clinical trials to compare rituximab against the standard of reference in each case, which should be used to define specific indications. With the level of current evidence, it seems reasonable to consider that rituximab is a therapeutic option for patients who have contraindications, intolerance or lack of response to conventional treatment regimens and for patients who have demonstrated dependence of calcineurin inhibitors and are exposed at the risk of chronic nephrotoxicity.

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