Abstract: SA-PO0731
A Diagnostic Challenge: Hepatitis C Virus (HCV)-Associated Membranoproliferative Glomerulonephritis in the Setting of Multiple Comorbidities
Session Information
- Glomerular Diseases: Complement-Mediated Glomerulopathies and Infection-Related GN
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Flowers, Addie, Texas Tech University System, Lubbock, Texas, United States
- Flores, Jackeline, Texas Tech University System, Lubbock, Texas, United States
- Natarajan, Piruthiviraj, Texas Tech University System, Lubbock, Texas, United States
- Yamaguchi, Leo, Texas Tech University System, Lubbock, Texas, United States
Introduction
Membranoproliferative Glomerulonephritis is an immune complex and/or complement mediated glomerular injury that occurs secondary to infection, autoimmune disease, malignancy, or idiopathic processes. We present a diagnostically challenging case in which the underlying etiology, and consequently management, was difficult to determine because of multiple coexisting conditions.
Case Description
A 59-year-old woman with significant PMH of hepatitis B/C non-compliant with treatment, retroperitoneal lymphadenopathy in the setting of unexplained weight loss concerning for an indolent lymphoma, CKD3b, and hypertension, presented for stroke-like symptoms secondary to a hypertensive emergency.
The hospital course was complicated by nephrotic range (UPCR 4.8 g/g) oliguric AKI, prompting a nephrotic work-up, revealing hypocomplementemia (C3 82 mg/dL, C4 7 mg/dL), chronic HBV (ALT 54 U/L, HBsAg +, HBeAg -, HBcAb IgM -. HBcAb IgG +, HBV DNA not detectable), active HCV infection (HCV RNA 112 IU/mL), and transiently positive cryoglobulins.
Renal biopsy demonstrated proliferative glomerulonephritis with IgM-dominant membranoproliferative features most consistent with HCV infection and/or cryoglobulinemia.
The nephrology team considered plasmapheresis and rituximab; however, due to transiently resolving cryoglobulins of unclear etiology, potential removal of antiviral medications, and concerns for hepatitis B reactivation in the setting of questionable medication compliance, both treatments were not pursued. The patient was ultimately treated with prednisone (~1mg/kg followed by a taper over 4 weeks), Entecavir, Epclusa, and discharged from the hospital.
Later, an EUS was performed with peri-pancreatic and peri-portal lymph node biopsies were negative for cancer along with a PET demonstrating low avidity in the concerning retroperitoneal lymph nodes. Oncology did not pursue lymph node biopsy due to the relatively small volume, stability in size, and belief that the retroperitoneal lymph nodes were likely reactive from chronic hepatitis and unlikely to be a lymphoproliferative disorder.
Discussion
MPGN is often driven by underlying immune complex or complement dysregulation, with infections such as hepatitis B and C being important treatable causes. Thorough evaluation for etiology is necessary, since management strategies differ and inappropriate treatment may worsen outcomes.