A 28-year-old man from rural Maharashtra presents with sudden onset gross hematuria and mild flank pain for 3 days. He recalls a sore throat 2 weeks prior that resolved spontaneously. On examination, BP is 148/92 mmHg, and mild periorbital edema is noted. Urine dipstick shows 3+ protein and RBCs with dysmorphic RBC casts. Serum creatinine is 1.4 mg/dL (baseline 0.9), and complement C3 level is low. What is the most likely diagnosis?

Explanation

## Clinical Presentation Analysis **Key Point:** The classic triad of post-streptococcal glomerulonephritis (PSGN) is: 1. Preceding streptococcal infection (pharyngitis or skin infection) 2. Latency period of 7–14 days 3. Sudden onset nephritic syndrome with hypertension and edema ## Diagnostic Features of PSGN | Feature | Finding in This Case | Significance | |---------|----------------------|--------------| | **Preceding infection** | Sore throat 2 weeks ago | Classic pharyngitis-associated PSGN | | **Latency period** | 14 days | Typical immune complex deposition lag | | **Presentation** | Gross hematuria, flank pain | Acute nephritic presentation | | **Hypertension** | 148/92 mmHg | Due to salt retention and volume expansion | | **Edema** | Periorbital | Characteristic of PSGN (vs. lower limb in nephrotic) | | **Urinalysis** | Dysmorphic RBC casts | Indicates glomerular bleeding | | **C3 complement** | Low | Immune complex activation (C3 dominant pattern) | | **Creatinine rise** | 1.4 from 0.9 | Mild renal impairment (usually reversible in PSGN) | ## Why PSGN and Not Alternatives **High-Yield:** PSGN is the most common nephritic syndrome in children and young adults worldwide, particularly in developing countries with high streptococcal infection burden. **Clinical Pearl:** The 1–2 week latency after pharyngitis is pathognomonic for PSGN. The low C3 with normal C4 (C3-dominant pattern) is the immunologic hallmark, reflecting classical pathway activation by immune complexes. ## Pathophysiology Streptococcal antigens (likely M protein) form circulating immune complexes → deposit in glomeruli → complement activation (C3 dominant) → inflammation → hematuria, proteinuria, and hypertension from salt/water retention. ## Expected Course - Spontaneous resolution in >95% of cases within 6–12 weeks - Proteinuria and hematuria gradually clear - Hypertension responds to salt restriction and diuretics - Prognosis excellent in children; adults may have slower recovery **Warning:** Do not confuse PSGN with IgA nephropathy (no preceding infection, episodic hematuria with upper respiratory illness, normal C3) or RPGN (rapidly progressive renal failure, ANCA positivity, crescent formation).