Tocilizumab-Induced Immune Complex Glomerulonephritis, or Is It?

Introduction: Takayasu Arteritis (TAK) is a vasculitis involving medium and large size blood vessels. TAK affects mostly women in their 40 to 50 years of age. Presents with limb claudication, pulseless extremities, and constitutional symptoms. Treatment includes corticosteroids plus disease modifying antirheumatic drugs (DMARDs). Tocilizumab (TCZ) is a biologic DMARD which targets interleukin 6 receptors to down regulate the inflammatory cascade. We present the case of a woman with TAK who was being treated with TCZ and subsequently developed immune complex glomerulonephritis (IC-GN). Case Description: A case of a 54-year-old female with history of TAK status post aortic bypass graft and left subclavian stenting maintained on TCZ, hypertension, diabetes mellitus type II, and chronic kidney disease stage IIIa, who presented having blood in her urine over two weeks. The patient was admitted for acute kidney injury. Laboratory work up with serum creatinine of 5.1mg/dL from a baseline of 1mg/dL. Urine protein-creatinine ratio of 2.8g/g from a baseline of no proteinuria. Urine microscopy with a new onset of red blood cells 50-100/high power field. Negative serologies: anti-nuclear antibodies, double stranded-DNA, myeloperoxidase, proteinase 3 antibodies, hepatitis panel and human immunodeficiency virus. Normal complement levels. Cryoglobulins were positive. Imaging was negative for any acute vascular disease. The kidney biopsy showed diffuse proliferative glomerulonephritis with a full house staining pattern on immunofluorescence with one glomerulus with a cellular crescentic lesion with fibrinoid necrosis. TCZ was held and pulse steroids started. It was followed by steroid taper and cyclophosphamide for 6 cycles. The patient became anuric and dialysis was initiated for solute and volume clearance. The patient remained dialysis dependent and unfortunately passed away from disseminated histoplasmosis after 6 months of treatment. Discussion: Our case of IC-GN in a patient with TAK that was being treated with TCZ, is a rare occurrence. It is unclear whether the IC-GN was TCZ induced, or a yet to be explained common immunological mechanism associated with TAK. This requires further studying of the association between TAK and different glomerulonephritis and further post marketing reporting of any unusual disease presentation in the setting of TCZ use.