Leishmaniasis-Associated Membranoproliferative Glomerulonephritis With Massive Complement Deposition

INTRODUCTION M embranoproliferative glomerulonephritis (MPGN) is a pattern of injury characterized by mesangial and endocapillary proliferation, double contours along the capillary walls, and lobular accentuation of the capillary tufts. Based on pathophysiology, MPGN is classified into MPGN mediated by immune complexes and Igs and complement-mediated MPGN. Immune complex/Ig–mediated MPGN most often results from an underlying infection, autoimmune disease, or monoclonal gammopathy. Complement-mediated MPGN includes C3 glomerulopathy, which encompasses C3 glomerulonephritis and dense deposit disease. C3 glomerulopathy is characterized by dominant staining for C3 and negative or minimal staining for Igs. The staining for C3 is at least 2 orders greater in magnitude than Ig staining. C3 glomerulopathy results from dysregulation of the alternative pathway of complement with accumulation of complement factors of the alternative and terminal pathways of complement. Infections are an important cause of MPGN that are usually associated with an immune complex–mediated MPGN. Immune complex–mediated MPGN due to infections is characterized by the presence of Ig, usually IgG or IgM, along with complement factors of the classical and terminal pathways. In this report, we present an unusual form of MPGN characterized by negative Ig but by large deposits of complement factors of the classical and terminal pathways in apatientwith leishmaniasis andHIV infection. Furthermore,Leishmania species amastigotesweredetected within macrophages in the interstitium. This finding of both complement-mediated MPGN and interstitial inflammation associated with leishmaniasis is extremely unusual and should be kept inmind as an uncommon cause of renal disease in the immunocompromised host.