## Diagnosis: Post-Streptococcal Glomerulonephritis (PSGN) The clinical and histopathological findings are diagnostic of PSGN: - Recent streptococcal infection (elevated ASO titre) - Nephritic presentation (hematuria, mild hypertension, proteinuria < 1 g/day) - Hypocomplementemia (low C3) - Endocapillary proliferation with subepithelial 'humps' (pathognomonic for PSGN) ## Treatment Strategy in PSGN **Key Point:** PSGN is a self-limited disease with spontaneous resolution in >95% of children and >50% of adults. The goal is supportive management and control of complications, NOT immunosuppression. **High-Yield:** The mainstay of treatment in PSGN is: 1. **Supportive care** — fluid restriction, diuretics for edema/hypertension 2. **ACE inhibitors/ARBs** — reduce proteinuria and slow progression 3. **Antihypertensives** — target BP control 4. **NSAIDs** — may be used cautiously for symptom relief **Clinical Pearl:** Corticosteroids are NOT routinely indicated in PSGN unless there is: - Rapidly progressive glomerulonephritis (RPGN) with crescent formation - Severe nephrotic syndrome with heavy proteinuria (>3.5 g/day) - Pulmonary hemorrhage or life-threatening extrarenal manifestations In this patient, the serum creatinine is only mildly elevated (1.2 mg/dL), proteinuria is mild (0.8 g/day), and there is no mention of crescents or systemic complications. Therefore, **supportive care with ACE inhibitors** is the appropriate first-line approach. ## Why Other Options Are Incorrect | Option | Why Not Used | |--------|-------------| | Corticosteroids alone | Not indicated in uncomplicated PSGN; reserved for RPGN or severe nephrotic syndrome | | Cyclophosphamide + corticosteroids | Reserved for ANCA-associated vasculitis, lupus nephritis, or RPGN; not first-line in PSGN | | Plasmapheresis | Indicated in anti-GBM disease or severe ANCA-associated vasculitis; no role in PSGN | [cite:Harrison 21e Ch 279]
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