De Novo C3 Glomerulonephritis of Allograft Associated With Factor H Autoantibody in a Patient with Systemic Lupus Erythematosus: A Case Report

Abstract

C3 Glomerulonephritis (C3GN) is a rare disease with a challenging diagnosis and poor prognosis. It is characterized by dysregulation of alternate complement pathway and diagnosed by biopsy findings of isolated or predominant C3 deposits on immunofluorescence (IF) staining. Dysregulation of alternate complement pathway (ACP) caused by genetic mutations or autoantibodies leads to C3 glomerulopathy (C3G) and complement-mediated thrombotic microangiopathies (c-TMA), later also referred to as atypical hemolytic uremic syndrome (aHUS). Autoantibodies like C3 nephritic factor and Factor H autoantibodies (FHAA) are frequently seen as acquired abnormalities in C3GN. SLE is a multisystem complex disorder distinguished by the presence of autoantibodies to multiple nuclear antigens, including DNA and ribonucleoprotein leading to complement activation, characterized by low level of C3 and C4 and may present with c-TMA. There are not many cases of C3GN with SLE that have been described, and current literature lacks strong evidence-based treatment options of post-transplant C3GN. Here, we describe a case of de novo C3GN of allograft in a patient with SLE.