S4845 C3 Glomerulonephritis: A Rare Presentation in the Setting of Infliximab Infusions for Ulcerative Pancolitis

Introduction: Infliximab (IFX), a tumor necrosis factor (TNF) monoclonal antibody, is a common treatment for ulcerative colitis (UC). Known side effects for UC patients receiving IFX include infections and infusion reactions. Glomerulonephritis in the setting of UC or TNF inhibitors is infrequently documented; to our knowledge there is minimal literature exploring complement component 3 (C3) glomerulonephritis adverse events. C3GN, a type of membranoproliferative glomerulonephritis, is caused by dysregulation in the alternative complement pathway. This case reports on a UC patient who developed C3GN after completing 3 IFX infusions. Case Description/Methods: A 46-year-old man with a history of UC diagnosed 1 year prior was hospitalized for acute kidney injury and hematuria. Previous UC regimen included IFX for 2 months before discontinuing treatment after experiencing an infusion reaction. At that time, patient’s creatine was 1.5, elevated compared to his baseline. He developed hematuria and was hospitalized 5 weeks later. During this admission, the patient had a creatine of 3 and the following unremarkable infectious work-up: blood cultures and hepatitis B/C testing. He also tested positive for perinuclear anti-neutrophil cytoplasmic antibodies with a low C3. A computed tomography of the abdomen and pelvis showed diffuse colonic wall thickening with adjacent inflammatory stranding and prominent lymph nodes consistent with pancolitis. The consequential renal biopsy revealed diffuse acute endocapillary proliferative glomerulonephritis with focal crescents and membranoproliferative glomerulonephritis features indicative of dominant C3GN. The patient was started on high-dose prednisone with significant improvement in symptomology. Discussion: C3GN is a novel process that was defined about fifteen years ago; consequentially, this pathology still requires investigation. While viruses and genetics are known contributors to C3GN, there are a few case reports describing ulcerative pancolitis with development of C3 glomerulopathy. Those patients had an acute decompensation of their UC and/or on a different biologic, such as mesalamine, contrary to this patient. Additionally, most of the literature associates TNF inhibitors with the far more common nephritic syndrome: IgA nephropathy. Highlighting C3GN in the context of infliximab treatments in a UC patient may draw attention to a potentially underreported adverse event and, consequently, contribute to the discussion of risks and surveillance in this population.