Abstract: TH-PO723
An Unusual Presentation of Poststreptococcal Glomerulonephritis (PSGN) in a Patient with Alcoholic Liver Cirrhosis
Session Information
- Glomerular Diseases: Case Reports - 1
October 24, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Zghayer, Aseel, Loyola University Chicago Stritch School of Medicine, Chicago, Illinois, United States
- Picken, Maria M., Loyola University Chicago Stritch School of Medicine, Chicago, Illinois, United States
- Leehey, David J., Loyola University Chicago Stritch School of Medicine, Chicago, Illinois, United States
Introduction
Post-infectious glomerulonephritis (PIGN) is commonly triggered by streptococcal skin or throat infections and is well-recognized to manifest in childhood. A characteristic feature of PIGN is the activation of the alternate complement pathway, leading to complement overactivation. The typical immunofluorescence pattern seen in PIGN is IgG and C3 deposition. Here, we present an unusual presentation of PIGN in a patient with liver cirrhosis following a recent streptococcal infection.
Case Description
A 54-year-old man, recently diagnosed with alcoholic liver cirrhosis, presented with abdominal pain attributed to an umbilical hernia. He developed oliguric acute kidney injury (AKI) necessitating hemodialysis. During further evaluation, the patient disclosed a history of sore throat, headache, and fever 2 weeks prior to admission. The workup is detailed in Table 1. Kidney biopsy demonstrated PIGN with prominent IgA as well as IgG deposition (Figure 1). After the biopsy, serology for anti-DNAse B was strongly positive, confirming a diagnosis of PSGN. Four weeks later, the C3 level had increased from < 15 to 56 mg/dL, and the patient is off dialysis with a serum creatinine of 2.0 mg/dL.
Discussion
Our patient's very low C3 and normal C4 levels make it highly unlikely that hypocomplementemia was due to a synthetic defect from hepatic cirrhosis. Given that patients with alcoholic liver disease are known to be at increased risk of PIGN, we hypothesize the possibility that our patient had an acute PSGN superimposed on a pre-existing IgA hepatic glomerulopathy. This case underscores the theory that patients with liver cirrhosis may have an impaired ability to clear immune complexes during bacterial infections.
Table 1. Work up
Figure 1.