Abstract: PUB207
Postinfectious Glomerulonephritis (PIGN) and Response to Steroids
Session Information
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Author
- Hussein, Hussein A., The University of Texas Medical Branch at Galveston, Galveston, Texas, United States
Introduction
Post-infectious glomerulonephritis (PIGN) is an immune complex-mediated glomerular disease that classically follows infections, particularly streptococcal infections. However, in adults, the clinical spectrum has expanded to include atypical presentations and a broader range of infectious triggers. C3 glomerulopathy (C3GN), characterized by predominant C3 deposition on renal biopsy, represents a distinct complement-mediated process but may overlap with PIGN in certain cases, complicating diagnosis and managemen
Case Description
A 37-year-old female with a history of alcohol dependence was brought to the Emergency Department after being found unresponsive by her mother, with an unknown downtime. Initial evaluation revealed acute kidney injury (AKI) with a creatinine of 8.6 mg/dL (baseline 0.6 mg/dL). Workup ruled out rhabdomyolysis (normal creatine kinase) and revealed leukocytosis (WBC 32,000) and proteinuria (uPCR 1.1 g). The patient was confused, weak, and a poor historian, but reported a history of bilateral lower extremity rash previously diagnosed as leukocytoclastic vasculitis via skin biopsy.
Her creatinine continued to rise, peaking at 9.6 mg/dL. Serologic workup for systemic connective tissue disease was negative (ANA negative, normal C3/C4). Renal ultrasound showed bilateral echogenic kidneys of normal size. A renal biopsy was performed, and the patient was started on pulse-dose intravenous methylprednisolone. Following the second dose of steroids, her creatinine began to trend downward, improving to 6.5 mg/dL.
Preliminary biopsy findings suggested post-infectious glomerulonephritis (PIGN), later confirmed on final pathology as acute post-infectious GN with C3 deposits. Given her steroid responsiveness, patient showed steady clinical improvement, with normalization of creatinine to 1.2 mg/dL at one month and to baseline (0.6 mg/dL) by three months. Notably, she did not develop significant edema or hematuria during the illness.
Discussion
Post-infectious GN, even in the setting of C3-dominant deposits, can be remarkably responsive to early pulse steroid therapy. A high index of suspicion, prompt renal biopsy, and early initiation of immunosuppression were critical in preventing irreversible renal failure. The patient’s history of alcohol dependence and poor clinical reliability could have delayed diagnosis, underscoring the need for aggressive early intervention in similar presentations.