# Case Report: A classical PSGN case with unusually prominent serosal manifestations and complement patterns that mimicked systemic autoimmune disease—highlighting diagnostic pitfalls and biopsy decision-making

## TL;DR

A rare case of post-streptococcal glomerulonephritis in a child presented with unusual serosal symptoms, mimicking autoimmune disease, highlighting the importance of careful diagnosis.

## Contribution

This case report highlights the rare occurrence of serosal involvement in pediatric PSGN and emphasizes diagnostic considerations to avoid unnecessary treatment.

## Key findings

- Serosal effusions (pleural and pericardial) were observed in a child with PSGN, a rare initial presentation.
- Conservative management led to full recovery without the need for immunosuppressive therapy.
- Low complement levels and resolution of symptoms confirm the self-limiting nature of PSGN.

## Abstract

Post-Streptococcal glomerulonephritis (PSGN) most commonly follows streptococcal infections and presents with classic features such as hematuria, proteinuria, hypertension, and transient renal dysfunction. While renal-limited disease is typical, extrarenal manifestations—particularly serosal involvement—are exceptionally rare in children.

We report a rare case of an adolescent who presented with nephritic syndrome marked by hypertension, gross hematuria, proteinuria, and notably, concurrent pleural and pericardial effusions. Laboratory evaluation revealed low serum complement levels (C3 and C4), consistent with immune complex-mediated glomerulonephritis. Extensive infectious and autoimmune workups were unremarkable. The patient was managed conservatively with antihypertensives and diuretics, with complete resolution of symptoms and normalization of renal function and complement levels within four weeks. To our knowledge, serosal involvement (pleural and pericardial effusions) at initial presentation in pediatric PSGN remains extremely rare, with very few documented cases in the literature. This report contributes valuable clinical insight, emphasizing that PSGN can occasionally mimic systemic inflammatory or autoimmune conditions. Early identification and conservative management can prevent overtreatment and improve outcomes.

This case underscores an unusual presentation of PSGN with serosal involvement—a manifestation reported only sporadically in literature. Recognition of such rare systemic features is crucial to avoid diagnostic delays or unnecessary immunosuppression. Supportive care alone led to favorable outcomes, reinforcing the self-limited nature of PSGN even in atypical presentations. It serves as a valuable reminder that atypical PSGN can present with multi-system inflammation, and a precise diagnostic approach integrating serology and clinical course is essential to avoid unnecessary intervention.