# Immunoglobulin A-Dominant Post-Infectious Glomerulonephritis Mimicking Henoch-Schönlein Purpura Nephritis in a Patient With Methicillin-Sensitive Staphylococcus aureus Bacteremia

## TL;DR

A patient with a staph infection and kidney damage was initially thought to have HSPN, but biopsy results showed IgA-PIGN, which has different treatment implications.

## Contribution

Highlights the diagnostic challenge and clinical distinction between IgA-PIGN and HSPN in the context of staphylococcal infection.

## Key findings

- IgA-PIGN was diagnosed via kidney biopsy, showing features distinct from HSPN.
- Steroid treatment was discontinued as IgA-PIGN may worsen with immunosuppression.
- The patient's renal function improved but was complicated by multi-organism bacteremia and duodenal perforation.

## Abstract

Staphylococcal infections remain a prominent cause of hospital- and community-acquired infections in the United States. Glomerulonephritis with predominant Immunoglobulin A (IgA) deposition following staphylococcal infection has been described as IgA-dominant postinfectious glomerulonephritis (IgA-PIGN). This clinical entity can mimic Henoch-Schönlein purpura nephritis (HSPN) given that it may also be preceded by staphylococcal infection, have similar kidney biopsy findings, and present with similar signs and symptoms.

Our patient presented with a palpable purpuric rash and acute kidney injury following methicillin-sensitive Staphylococcus aureus (MSSA) bacteremia treated with intravenous cefazolin. A skin biopsy revealed leukocytoclastic vasculitis and vascular IgA deposition. Urinalysis showed active urinary sediment with hematuria and proteinuria. These findings were concerning for possible HSPN that was triggered by either staphylococcal infection or antibiotic exposure. Given worsening renal injury, the patient was started on empiric methylprednisone while awaiting kidney biopsy. When performed, the findings of diffuse proliferative glomerulonephritis with exudative features, subepithelial and mesangial deposits with strong C3 and moderate IgA staining were more consistent with IgA-PIGN over HSPN. Since IgA-PIGN is not responsive to steroids and may in fact be worsened by immunosuppression, methylprednisone was discontinued. The patient’s renal function improved; however, he developed multi-organism bacteremia and duodenal perforation, ultimately leading to death.

This case demonstrates the importance of distinguishing IgA-PIGN from HSPN in a patient with Staphylococcal infection presenting with renal injury and purpuric rash. Characteristic clinical signs and renal biopsy findings may aid in differentiating the two clinical entities so that the appropriate treatment can be initiated.