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 markedly in high-income countries, attributed to improved living conditions, hygiene, and access to care; antibiotic treatment of the index infection has not been shown to prevent PSGN. 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?
AThin basement membrane disease
BMembranoproliferative GN
CLupus nephritis
DIgA nephropathy
EPost-infectious glomerulonephritis
Reveal answer & full explanation
Correct answer: E — Post-infectious glomerulonephritis
AThin basement membrane disease
BMembranoproliferative GN
CLupus nephritis
DIgA nephropathy
EPost-infectious glomerulonephritis✓
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) and anti-DNase B confirm recent group A strep infection; anti-DNase B rises after both pharyngeal and skin infection, whereas the ASO response is often blunted after skin infection
Why the others are wrong
IgA nephropathy — IgA nephropathy presents with synpharyngitic hematuria (concurrent with, not 1-3 weeks after, infection) and typically does not cause low complement
Lupus nephritis — lupus nephritis consumes both C3 and C4; this patient has normal C4, making lupus less consistent
Thin basement membrane disease — causes persistent microscopic hematuria without significant proteinuria, complement abnormalities, or post-infectious timing
Membranoproliferative GN — a low C3 with normal C4 can also occur in MPGN, but the 10-day latent period after pharyngitis with elevated ASO and anti-DNase B fits PSGN, whose C3 typically normalizes within 6-8 weeks; hypocomplementemia persisting beyond that suggests MPGN or C3 glomerulopathy
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 9-year-old girl develops cola-colored urine and periorbital edema 11 days after streptococcal pharyngitis. Her blood pressure is 134/88 mm Hg, urinalysis shows red cell casts, and serum C3 is low. Which of the following is true of this condition but not of acute rheumatic fever?
AIt begins after a latent period following the streptococcal infection
BIt has not been shown to be prevented by treating the infection
CIt frequently recurs with subsequent streptococcal infections
DIt is caused by antibodies that cross-react with host tissue proteins
EIt has not been linked to elevated antistreptococcal antibody titers
Reveal answer & full explanation
Correct answer: B — It has not been shown to be prevented by treating the infection
AIt begins after a latent period following the streptococcal infection
BIt has not been shown to be prevented by treating the infection✓
CIt frequently recurs with subsequent streptococcal infections
DIt is caused by antibodies that cross-react with host tissue proteins
EIt has not been linked to elevated antistreptococcal antibody titers
Why It has not been shown to be prevented by treating the infection is correct
This is post-streptococcal glomerulonephritis (PSGN): nephritic syndrome (cola-colored urine, edema, hypertension, RBC casts) with a low C3, arising 11 days after group A streptococcal (GAS) pharyngitis.
Antibiotic treatment of GAS pharyngitis or skin infection has not been shown to prevent PSGN (IDSA GAS pharyngitis guideline; CDC), so a history of a treated sore throat does not lower suspicion for it.
Acute rheumatic fever (ARF) is the opposite: penicillin or amoxicillin started within 9 days of sore-throat onset prevents a first attack (AHA 2009, IDSA 2012), and preventing ARF is a principal reason to test for and treat GAS pharyngitis.
Once PSGN is diagnosed, CDC still advises penicillin (preferably penicillin G benzathine) to eradicate any remaining GAS and help prevent spread to other people, not to change the renal course.
Why the others are wrong
It begins after a latent period following the streptococcal infection - True of PSGN (about 10 days after pharyngitis, about 3 weeks after skin infection), but equally true of ARF, which appears about 2-4 weeks after GAS pharyngitis; the latency separates both from IgA nephropathy, whose hematuria is synpharyngitic, not PSGN from ARF (the trap is confirming a true PSGN fact from the vignette without checking the ARF half of the lead-in).
It frequently recurs with subsequent streptococcal infections - Recurrence of PSGN is rare, and long-term antibiotic prophylaxis is not recommended after it; ARF is the condition that carries a high risk of recurrence with later GAS infections, greatest in the first few years after the first attack, which is why ARF survivors receive secondary prophylaxis for at least 5 years or until age 21, whichever is longer, and longer after carditis (the trap is carrying the ARF prophylaxis rule over to the kidney).
It has not been linked to elevated antistreptococcal antibody titers - False of both: elevated titers are standard supporting evidence in PSGN (antistreptolysin O after pharyngitis; anti-DNase B after pharyngitis or skin infection, because the ASO response is weak after impetigo), and the revised Jones criteria for ARF require evidence of a preceding GAS infection, most often an elevated or rising ASO or anti-DNase B titer (isolated Sydenham chorea, with its long latency, is the usual exception) (the trap is stretching the low-ASO-after-impetigo rule into a claim that PSGN lacks antibody evidence).
It is caused by antibodies that cross-react with host tissue proteins - both are immune-mediated nonsuppurative sequelae, which makes this tempting, but antibodies that cross-react with host proteins such as cardiac myosin (molecular mimicry, type II hypersensitivity) are the proposed mechanism of ARF; PSGN is an immune-complex (type III) glomerulonephritis that consumes complement, which is why this child's C3 is low (the trap is assigning one autoimmune mechanism to every post-streptococcal disease).
Additional high-yield points
Treat GAS pharyngitis to prevent ARF with penicillin V or amoxicillin for 10 days, or a single IM dose of benzathine penicillin G.
Both are nonsuppurative sequelae: the host immune response, not bacteria in the kidney or heart, causes the injury. ARF is thought to arise from antibodies to streptococcal antigens that cross-react with host proteins such as cardiac myosin (molecular mimicry, type II hypersensitivity), whereas PSGN is an immune-complex (type III) glomerulonephritis that consumes complement, which is why this child's C3 is low.
PSGN follows both pharyngitis and skin infection such as impetigo; ARF is classically taught as a sequela of pharyngitis only, although CDC now also links it to skin infection.
PSGN care is supportive: sodium and fluid restriction plus a loop diuretic for edema and hypertension. More than 90% of children recover fully, whereas ARF can leave chronic rheumatic heart disease.
C3 usually normalizes within 6-8 weeks and should do so by 12 weeks; a C3 still low beyond that points toward C3 glomerulopathy/MPGN or lupus nephritis rather than PSGN.
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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 (alternative-pathway consumption) — characteristic but not specific (also seen in C3 glomerulopathy and some MPGN); usually normalizes within 6-8 weeks
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 biopsy for an alternative diagnosis (C3 glomerulopathy, MPGN, lupus)
Family screening of household contacts for active strep infection
Adults: 25-50% may have persistent abnormalities (proteinuria, hypertension, CKD)
Children: excellent prognosis with >95% complete recovery
PANCE pearls
Low C3 + normal C4 is the classic complement signature; should normalize within 6-8 weeks. C3 still low beyond 8-12 weeks → biopsy for C3 glomerulopathy or MPGN (lupus usually lowers C4 as well).
ASO titer rises after pharyngitis but not reliably after skin infection — order anti-DNase B for impetigo-associated cases.
Antibiotics for the strep infection do NOT prevent or alter PSGN (unlike rheumatic fever, which IS prevented by antibiotics).
Children have excellent prognosis; adults have worse outcomes with 25-50% having residual abnormalities.
Hematuria can persist for months; proteinuria may persist longer. Hypertension and edema typically resolve within 1-2 weeks.
References
KDIGO 2021 — KDIGO 2021 Clinical Practice Guideline for the Management of Glomerular Diseases
Eison 2011 — Post-streptococcal acute glomerulonephritis in children (Eison et al., Pediatr Nephrol 2011)
Rodríguez-Iturbe — Rodríguez-Iturbe B, Musser JM. The current state of poststreptococcal glomerulonephritis. J Am Soc Nephrol. 2008;19(10):1855-1864.
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