Rituximab induces regression of hepatitis C virus-related membranoproliferative glomerulonephritis in a renal allograft

Abstract

Hepatitis C virus (HCV) infection complicates clinicaloutcome in liver and renal allografts [1]. Besides itsimportant contribution to chronic liver disease, HCVinfection is also a relevant cause of de novo immune-mediated glomerulonephritis in both kidney and livertransplantation [2,3]. It has been shown that thedevelopment of de novo membranous and especiallymembranoproliferative glomerulonephritis (MPGN)in renal allografts is strongly associated with pre-transplant HCV-positive serology. It has also beendemonstrated that type I MPGN is mediated by a verylow level of nephritogenic type II cryoglobulinscontaining HCV-RNA [4]. Those lesions induce anaccelerated loss of the graft [5].Antiviral treatment for HCV-infected renal trans-plant candidates with interferon- (IFN- ) prior totransplantation is strongly recommended, since theclearance of HCV-RNA is beneficial for post-trans-plant liver disease [6] and to prevent HCV-relatedglomerulonephritis [7]. Nevertheless, 30–50% ofpatients do not tolerate or do not respond to IFN- ,thus continuing at risk for HCV-related glomerulone-phritis. Furthermore, there is neither an effective nor asafe therapy for HCV-related glomerular lesions aftertransplantation; ribavirin-based therapy has shownsome severe adverse events [8] and Interferon-alpha(INF- ) can induce graft dysfunction or rejection [9].Hence, it is important to explore new therapeuticapproaches to treat this deleterious complication.In this article, we report a case of HCV-relatedMPGN in a renal allograft treated with anti-CD20monoclonal antibodies. We describe for the first timeregression of glomerular subendothelial immunedeposits and we discuss the virological and immuno-logical changes induced by this treatment.