Abstract: SA-PO0713
Posterior Encephalopathy Syndrome (PRES) in Hepatitis C Virus (HCV)-Associated Seronegative Cryoglobulinemia and Active Hepatitis C: A Diagnostic and Therapeutic Challenge
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
- Imtiaz, Syeda H., Southeast Health, Dothan, Alabama, United States
- Naveed, Osama Kunwer, Southeast Health, Dothan, Alabama, United States
Introduction
PRES is a rare CNS manifestation of cryoglobulinemia. While hypertension is a known cause in this setting, vasculitis is emerging as an underrecognized trigger. Distinguishing hypertensive from vasculitis-mediated PRES is a diagnostic and therapeutic challenge in the setting of seronegative cryoglobenemia and active Hepatitis C.
Case Description
A 41-year-old female with HCV-associated biopsy-proven cryoglobulinemia presented with seizures, headache, confusion and BP 210/140. She had received four doses of rituximab and steroids for cryoglobulinemic glomerulonephritis five weeks prior, but was lost to follow-up. Brain MRI showed bilateral parieto-occipital FLAIR hyperintensities without diffusion restriction and increased ADC signal, consistent with PRES. MRA showed no bead-on-string appearance; however, small-vessel vasculitis could not be excluded, as contrast studies were deferred due to AKI. Labs revealed AKI with active sediment (100 RBC, 3+ protein), normal C3 (87 mg/dL), low C4 (10 mg/dL), high RF (156 IU/mL), HCV RNA 7,170,000 IU/mL and undetectable serum cryoglobulins despite prior biopsy-proven disease. Management included aggressive BP control, antiepileptics, and diuresis. AKI resolved within three days. Immunosuppression and CSF analysis were deferred given high-titer active HCV, clinical improvement and classic PRES pattern on MRI. Outpatient direct acting antiviral (DAA) therapy was recommended.
Discussion
This case highlights the diagnostic complexity of ruling out vasculitis-associated PRES in the context of seronegative cryoglobulinemia, limited small-vessel imaging, and absence of CSF studies, as well as the therapeutic challenge of initiating immunosuppressive therapy while weighing the risks given active Hepatitis C infection. Current guidelines recommend combining DAAs with rituximab for severe HCV-associated cryoglobulinemic vasculitis; however, in this patient, given improvement with BP control alone, the absence of progressive or life-threatening organ involvement, and the elevated risk of infection with high-titer active HCV, immunosuppression was deferred in favour of outpatient DAA therapy. This case underscores the need for a decision-making framework when managing PRES in seronegative cryoglobulinemic vasculitis with concurrent active HCV.