A Case of DNAJB9 with rapid renal progression to End-Stage Renal Disease in a patient with previously treated HCV Background Fibrillary glomerulonephritis (FGN) is a rare and progressive kidney disease, accounting for 0.5% to 1.4% of native kidney biopsies. It is characterized by non-amyloid fibrillar deposits in the extracellular matrix. Although historically regarded as idiopathic, recent studies have revealed associations with autoimmune diseases, malignancies, and Hepatitis C virus (HCV) infection. DNAJB9, a proteomic marker identified through mass spectrometry, has been consistently found in FGN cases, regardless of congophilia. This case illustrates FGN in a patient with a history of successfully treated Hepatitis C, with rapid progression to end-stage renal disease (ESRD). Case Presentation A 54-year-old female with a medical history of successfully treated Hepatitis C (using Glecaprevir and Pibrentasvir), cerebrovascular accident (CVA), coronary artery disease (CAD), decompensated cirrhosis, and chronic kidney disease (CKD) presented with encephalopathy. Upon admission, her vital signs were stable (blood pressure 118/64 mmHg, heart rate 73 bpm, respiratory rate 22 breaths/min, oxygen saturation 99% on room air). Physical examination revealed an obese abdomen with significant ascites but no asterixis, tremor, or skin lesions. Laboratory results showed acute kidney injury (serum creatinine 9.24 mg/dL, blood urea nitrogen 103 mg/dL, ammonia 106 µmol/L), with preserved synthetic liver function (INR 1.2). Urinalysis was negative for microscopic hematuria. During a previous admission, the patient's serum creatinine level was 5.9 mg/dL, highlighting a rapid decline in renal function. Serological tests were negative for hepatitis B, C, HIV, autoimmune markers, and monoclonal spikes. Imaging showed no evidence of hydronephrosis. The etiology of CKD was believed to be multifactorial but her current presentation prompted further diagnostic biopsy. A renal biopsy showed immune deposits with a fibrillary substructure on electron microscopy, while immunohistochemistry confirmed the presence of DNAJB9, solidifying the diagnosis of FGN. Light microscopy revealed over 40% of moderate tubular atrophy and, interstitial fibrosis, and mild non-specific inflammation. Immunofluorescence microscopy was negative for IgG, IgA, IgM, C1q, albumin, fibrinogen, and kappa/lambda light chains. The patient met indications for renal replacement therapy and was started on hemodialysis. She underwent paracentesis with albumin infusion as needed. No renal recovery was observed. Discussion This case illustrates a patient with previously treated hepatitis C and worsening renal function. We suspect this pathologic process had been ongoing for months but by the time the biopsy was done the damage was irreversible. The patient's history of treated HCV points out the risk of renal involvement and GN developing later on despite on successful HCV treatment. Conclusion FGN should be considered in the differential diagnosis for any patients with rapidly declining renal function, even in the absence of typical signs of glomerulonephritis. DNAJB9 serves as a novel diagnostic marker for FGN. Prior Hepatitis C infection continues to be a significant risk factor for FGN and renal disease progression.