Immune complex GN 1-3 weeks after group A strep pharyngitis or impetigo.
Also known as: PSGN, post-streptococcal GN, acute post-infectious GN
Overview
An immune complex-mediated glomerulonephritis occurring 1-3 weeks after infection with nephritogenic strains of group A beta-hemolytic streptococcus (GAS), typically pharyngitis or skin infection (impetigo). Presents with classic nephritic syndrome.
Epidemiology
Most common cause of acute glomerulonephritis in children worldwide. Peak age 4-12 years. Incidence has declined in developed countries with early antibiotic treatment of strep infections. Adults can be affected, with worse prognosis. Outbreaks may follow skin infection epidemics.
Try two board-style Post-Streptococcal Glomerulonephritis questions
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Question 1RenalEasy
A 25-year-old female has cola-colored urine 10 days after a sore throat. Urine dipstick shows 3+ protein and 3+ blood. Urine microscopy shows RBC casts and dysmorphic RBCs. Serum C3 is markedly reduced and C4 is normal. Serum creatinine is 1.6. Streptococcal antibodies (antistreptolysin O (ASO) and anti-DNase B) are elevated. Which of the following is the most likely diagnosis?
APost-infectious glomerulonephritis
BIgA nephropathy
CLupus nephritis
DThin basement membrane disease
Reveal answer & full explanation
Correct answer: A — Post-infectious glomerulonephritis
APost-infectious glomerulonephritis✓
BIgA nephropathy
CLupus nephritis
DThin basement membrane disease
Why Post-infectious glomerulonephritis is correct
Post-streptococcal glomerulonephritis (PSGN) is an immune complex-mediated glomerulonephritis (GN) occurring 1-3 weeks after Group A Strep pharyngitis (or 3-6 weeks after skin infection)
Complement pattern: low C3 (alternate pathway activation and consumption) with NORMAL C4 — this distinguishes PSGN from lupus nephritis, which consumes both C3 and C4
Elevated antistreptolysin O (ASO) confirms pharyngeal strep; anti-DNase B is elevated after skin infection
Why the others are wrong
B) IgA nephropathy — IgA nephropathy presents with synpharyngitic hematuria (concurrent with, not 1-3 weeks after, infection) and typically does not cause low complement
C) Lupus nephritis — lupus nephritis consumes both C3 and C4; this patient has normal C4, making lupus less consistent
D) Thin basement membrane disease — causes persistent microscopic hematuria without significant proteinuria, complement abnormalities, or post-infectious timing
Additional high-yield points
Treatment is supportive: antihypertensives, loop diuretics for edema, salt restriction
Prognosis: most children recover completely; 50% of adults may have persistent proteinuria or hypertension
Antibiotics: treat active strep infection if still present
Question 2RenalMedium
A child develops cola-colored urine and edema two weeks after streptococcal pharyngitis. Which of the following best explains the mechanism?
APodocyte foot process effacement without deposits
BImmune complex deposition in glomeruli
CAnti-glomerular basement membrane antibodies
DMesangial IgA deposition during active infection
Reveal answer & full explanation
Correct answer: B — Immune complex deposition in glomeruli
APodocyte foot process effacement without deposits
BImmune complex deposition in glomeruli✓
CAnti-glomerular basement membrane antibodies
DMesangial IgA deposition during active infection
Why Immune complex deposition in glomeruli is correct
Post-streptococcal glomerulonephritis is driven by deposition of strep-antigen immune complexes in the glomerulus with complement activation.
The 2-week latent period after pharyngitis, cola-colored urine, edema, and low complement are classic.
Subepithelial humps on electron microscopy confirm the immune-complex mechanism.
Why the others are wrong
Mesangial IgA deposition during active infection — IgA nephropathy causes hematuria within days of a URI (synpharyngitic), not after a 2-week latent period; the timing here points away from it.
Anti-glomerular basement membrane antibodies — Anti-GBM (Goodpasture) disease produces rapidly progressive nephritis with pulmonary hemorrhage, not a self-limited post-strep picture in a child.
Podocyte foot process effacement without deposits — That describes minimal change disease, a nephrotic process with heavy proteinuria, not the nephritic cola-colored hematuria seen here.
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Nephritogenic strains of GAS (M types 1, 4, 12 in pharyngitis; M types 47, 49, 55 in impetigo) produce antigens (notably streptococcal pyrogenic exotoxin B and nephritis-associated plasmin receptor) that form circulating immune complexes or deposit in situ in subepithelial glomerular sites. Complement activation (alternative pathway predominantly) drives inflammation, mesangial and endothelial proliferation.
Clinical presentation
Symptoms
Abrupt onset of tea-colored or cola-colored urine (gross hematuria) 1-3 weeks after pharyngitis or 3-6 weeks after impetigo
Periorbital edema, especially in the morning
Decreased urine output
Headache and malaise from hypertension
Children may have nonspecific symptoms initially
Signs / physical exam
Hypertension (50-90% of children)
Periorbital and dependent edema
Tea-colored or smoky urine
Mild tenderness over flanks (uncommon)
Healed strep infection — pharyngeal exam often normal at presentation
Classic findings
Cola-colored urine + periorbital edema + hypertension in a child 1-3 weeks after sore throat or impetigo = classic PSGN.
Differential diagnosis
IgA nephropathy — Synpharyngitic hematuria (within 1-3 days, not 1-3 weeks); normal complement; recurrent episodes
Other post-infectious GN — After staph, gram-negative, or viral infections; similar pathology
Diagnostic workup
Diagnostic criteria
Clinical diagnosis: nephritic syndrome + recent strep infection + low C3 + positive streptococcal serology. Biopsy reserved for atypical presentations (persistent low C3 >8 weeks, severe AKI, RPGN features) and shows endocapillary proliferative GN with subepithelial 'humps' on EM and granular IgG/C3 on IF.
Labs
Urinalysis: hematuria with dysmorphic RBCs and RBC casts, mild-moderate proteinuria (typically subnephrotic), pyuria
BMP: elevated creatinine, sometimes hyperkalemia
Low C3 (90%), normal C4 — pathognomonic complement pattern
Streptococcal serologies: ASO (positive in 60-80% after pharyngitis but less so after skin infection), anti-DNase B (more sensitive after impetigo), anti-hyaluronidase, anti-streptokinase
Throat culture or skin culture (often negative by time of GN presentation)
Streptozyme test combines multiple antibodies
Imaging
Renal ultrasound usually unnecessary; normal or mildly enlarged kidneys
Diagnostic algorithm
Feature
PSGN
IgA Nephropathy
Latency after infection
1-3 wk (pharyngitis); 3-6 wk (skin)
1-3 days (synpharyngitic)
Age
Children 4-12 yr (mainly)
Young adults
Complement C3
Low (resolves in 6-8 wk)
Normal
Serology
ASO, anti-DNase B positive
Elevated IgA (~50%)
Course
Self-limited (children); residual in adults
Chronic, relapsing
Biopsy IF
Granular IgG/C3, 'humps' on EM
Mesangial IgA deposits
Prognosis
>95% recovery in children
20-40% ESRD over 20 yr
Distinguishing post-streptococcal GN from IgA nephropathy — the two most common pediatric/young adult nephritic presentations.
Treatment
First-line
Supportive care — most cases resolve spontaneously
Sodium and fluid restriction for volume overload
Loop diuretic — furosemide — for edema and hypertension
Antihypertensives: CCB (amlodipine) or ACEi (if renal function stable); hydralazine or nicardipine for hypertensive emergency
Antibiotics (penicillin V, amoxicillin, or erythromycin if allergic) if active strep infection still present — does NOT alter renal course but limits transmission
Second-line / adjunct
Dialysis temporarily if severe AKI with hyperkalemia, uremia, or refractory volume overload (rare)
Glucocorticoids only if biopsy shows crescents (atypical RPGN course)
Monitor C3 — should normalize within 6-8 weeks; persistent low C3 should prompt alternative diagnosis (MPGN, lupus)
Family screening of household contacts for active strep infection
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