Abstract: TH-PO091
Navigating Challenges: A Case of IgA-Dominant Postinfectious Glomerulonephritis
Session Information
- AKI: Clinical, Outcomes, and Trials - Epidemiology and Pathophysiology
October 24, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Dalal, Aashvi R., NewYork-Presbyterian Brooklyn Methodist Hospital, Brooklyn, New York, United States
- Liben, Michael, NewYork-Presbyterian Brooklyn Methodist Hospital, Brooklyn, New York, United States
- Villareal, Ronald D., NewYork-Presbyterian Brooklyn Methodist Hospital, Brooklyn, New York, United States
Introduction
IgA-dominant postinfectious glomerulonephritis (IgA-PIGN) a variant of Acute Post Infectious Glomerulonephritis is caused by immune complexes that deposit in the glomeruli with dominance or codominance of IgA with C3. Commonly associated with gram-positive infections, especially in elderly and diabetic population, it manifests as renal dysfunction, hematuria, and proteinuria. Here, we present a case highlighting diagnostic and treatment challenges in IgA-PIGN.
Case Description
A 63-year-old male with congestive heart failure, hypertension, type 2 DM, and CKD stage 4 presented to the hospital for evaluation of fever and purulent left foot ulcer. Recent previous hospitalisation involved left food osteomyelitis complicated by MSSA bacteremia. Lab results revealed leukocytosis (12.85 x 103 /ul), hyperkalemia (6.1mmol/L) and elevated creatinine (7.29 mg/dl with baseline 2-3 mg/dl). Urinalysis showed >100 rbc/hpf, and >300 mg/dl protein with UPCR of 4.4 gm. C3, C4, ANA, ANCA, and hepatitis panel were unremarkable. Renal biopsy confirmed IgA dominant mesangial immune complex disease, post infectious, cellular crescents with severe acute interstitial nephritis (AIN). Granular pattern seen for 1+ IgA and 2+ C3 on immunofluorescence. On Electron Microscopy, increase in mesangial matrix and electron dense deposit was noted. Hemodialysis was initiated due to worsening kidney function. Since infection was the culprit, antibiotics were continued and steroids were initially withheld. However, prednisone was later started due to AIN findings, with reassuring evidence of negative blood cultures and no evidence of endocarditis on echocardiogram. Partial recovery led to discharge on hemodialysis with tapering steroids.
Discussion
Distinguishing IgA-PIGN from IgA nephropathy is crucial as treatments and prognosis differ. While IgA nephropathy warrants immunosuppression, IgA-PIGN relies on antibiotics for underlying infection management. As seen with this patient, challenges arose in initiating steroids due to concurrent AIN. This case highlights the need to consider IgA-dominant PIGN in sepsis patients with worsening renal function, often misdiagnosed as acute tubular necrosis or ischemic injury. Importance of high clinical suspicion in the prompt diagnosis in infection-related AKI is crucial for accurate diagnosis and intervention of IgA-dominant APIGN.