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Fibrillary glomerulopathy is an uncommon cause of progressive kidney disease, and the development of superimposed crescentic glomerulonephritis creates a particularly difficult therapeutic challenge.We report an 84-year-old woman with progressive kidney dysfunction, persistent hematuria, and proteinuria.Over 12 months, serum creatinine increased from 0.99 mg/dL to 2.52 mg/dL, with estimated glomerular filtration rate declining from 57 mL/min/1.73m² to approximately 18 mL/min/1.73m².Serologic evaluation, including antinuclear antibody, antineutrophil cytoplasmic antibody, and complement levels, was unrevealing, and evaluation for monoclonal gammopathy was negative.Kidney biopsy demonstrated DNAJB9-negative fibrillary glomerulopathy with superimposed focal crescentic glomerulonephritis.The patient was initially treated with prednisone 80 mg daily, and avacopan was started at a dose of 30 mg twice a day two weeks after initiation of prednisone therapy.The prednisone dose was rapidly tapered, and avacopan was subsequently used as a glucocorticoid-sparing strategy.At 12 months, kidney function remained stable, with serum creatinine of 1.97 mg/dL without progression to dialysis-dependent kidney failure.Early biopsy and individualized immunosuppressive therapy are critical, and emerging agents such as avacopan may offer glucocorticoid-sparing benefits in selected cases.
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Kamath et al. (2026) studied this question.
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