Full‐House Nephropathy Without Lupus Manifesting During Acute Kidney Allograft Rejection: A Case Report

Kidney transplantation increases the survival rate of end-stage renal disease patients; however, acute rejection and glomerulonephritis, such as the uncommon non-lupus full-house nephropathy (NLFHN), can lead to graft dysfunction. NLFHN exhibits a characteristic lupus immunofluorescence pattern in the absence of systemic lupus features, which makes both diagnosis and treatment more challenging for transplant recipients. A 34-year-old female with a background of ABO-compatible living-related kidney transplantation presented 12 years after the transplant with worsening hypertension, elevated serum creatinine (1.9 mg/dL), and subnephrotic range proteinuria. Biopsy of kidney revealed Non-lupus full-house nephropathy (NLFHN) accompanied by T-cell-mediated rejection. Immunofluorescence showed a "full-house" pattern (IgG, IgA, IgM, C3, and C1q) in the absence of systemic lupus erythematosus (SLE) features (negative ANA, normal C3). Despite intensified immunosuppressive treatment, proteinuria persisted, highlighting challenges in managing overlapping immune-mediated kidney pathologies. The simultaneous presentation of acute rejection and NLFHN indicates a complex interplay between alloimmune injury and immune complex deposition, contributing to graft damage. Management of this challenge, due to limited treatment options and variable responses, highlights the necessity for early detection and further research aimed at improving outcomes.