Poststreptococcal Glomerulonephritis
The most likely diagnosis is (C) Poststreptococcal glomerulonephritis (PSGN), given the classic presentation of nephritic syndrome (hematuria, edema, hypertension) occurring 1-3 weeks after untreated streptococcal pharyngitis. 1
Clinical Reasoning
This patient presents with the pathognomonic triad that distinguishes PSGN from the other options:
- Temporal relationship: Sore throat "a few weeks ago" followed by renal manifestations is the classic 1-3 week latency period between streptococcal pharyngitis and PSGN 1, 2
- Nephritic syndrome: The combination of bloody urine (hematuria), significant lower extremity edema, and hypertension (166/108 mmHg) represents acute glomerulonephritis 1, 3
- Untreated infection: The pharyngitis was neither examined nor treated, allowing progression to this immune-mediated complication 1
Why Not the Other Options?
IgA nephropathy (Berger disease) - Options A and B are the same condition:
- IgA nephropathy typically presents with episodic gross hematuria occurring simultaneously with or within 1-2 days of an upper respiratory infection, not weeks later 4
- The timing in this case (weeks after pharyngitis) excludes IgA nephropathy 4
Membranous glomerulonephritis:
- Presents with nephrotic syndrome (heavy proteinuria, hypoalbuminemia, hyperlipidemia) rather than nephritic syndrome 4
- Does not have the characteristic temporal relationship with streptococcal infection 4
- Typically lacks the acute hypertension and hematuria seen here 4
Diagnostic Confirmation
If you were to confirm this diagnosis, you would expect:
- Serologic evidence: Elevated anti-streptolysin O (ASO) titers or anti-DNAse B antibodies 1, 3
- Complement studies: Low C3 complement levels (hallmark finding) with normal C4 1, 3
- Urinalysis: Dysmorphic red blood cells, red cell casts, and moderate proteinuria (1-3 g/day) 3
- Tea-colored urine: Characteristic appearance with proteinuria >2+ by dipstick 4, 3
Key Clinical Pitfall
Do not be misled by the absence of active pharyngitis at presentation. PSGN is an immune complex-mediated disease that develops 1-3 weeks after the initial streptococcal infection, when the infection itself may have already resolved 1, 2. The immune complexes deposit in glomerular tissue causing inflammation and kidney damage even without ongoing infection 1.
Expected Clinical Course
PSGN typically has excellent prognosis with supportive care, including sodium restriction, diuretics for edema and hypertension management, and antibiotics (penicillin or erythromycin if penicillin-allergic) to decrease antigenic load 1. C3 complement levels should normalize within 8-12 weeks; persistent low C3 beyond 12 weeks would warrant kidney biopsy to exclude other diagnoses 1, 3.