Post streptococcal glomerulonephritis
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Post-Streptococcal Glomerulonephritis (PSGN)
Definition & Overview
PSGN is a postinfectious, immune complex–mediated glomerulonephritis that follows skin (impetigo) or throat (pharyngitis) infection by nephritogenic strains of Group A β-hemolytic streptococci (S. pyogenes). Occasionally Groups C or G streptococci are implicated. It is the prototype of the nephritic syndrome and of immune complex glomerulonephritis.
Epidemiology
| Feature | Detail |
|---|---|
| Incidence | ~9/100,000/year in developing countries; declining in developed nations |
| Age | Primarily children 2–18 years; severe adult disease documented |
| Sex | Male : Female = 2 : 1 |
| Form | Epidemic (after pharyngitis outbreaks) or sporadic |
| Subclinical : Clinical ratio | 4–5 : 1 (microscopic hematuria + ↓complement only) |
Pathogenesis
PSGN is an acute immune complex disease:
- Nephritogenic strains of Group A strep produce antigens (e.g., nephritis-associated plasmin receptor [NAPlr], streptococcal pyrogenic exotoxin B [SpeB])
- Host forms antibodies against these streptococcal antigens
- Immune complexes deposit (or form in situ) in glomerular capillary walls
- Complement activation (classic pathway) → consumption of C3 (↓ in >90% of cases)
- Inflammatory response: infiltration of monocytes and PMNs → glomerular injury
Latent Period
| Site of Infection | Latent Period |
|---|---|
| Throat (pharyngitis) | 7–10 days (some say 10–14 days) |
| Skin (impetigo/pyoderma) | 2–4 weeks |
This latent period distinguishes PSGN from IgA nephropathy (which has synpharyngitic hematuria, i.e., concurrent or within 1–2 days).
Clinical Presentation
The classic presentation is acute nephritic syndrome:
| Feature | Details |
|---|---|
| Hematuria | Gross (tea/cola-colored urine) or microscopic; RBC casts pathognomonic |
| Proteinuria | Usually sub-nephrotic; occasionally nephrotic-range |
| Hypertension | Due to sodium/water retention |
| Edema | Facial (periorbital) and peripheral — from salt/water retention |
| Oliguria | Reduced urine output |
| Azotemia | Elevated BUN and creatinine (more common and severe in elderly) |
Rare presentations:
- Nephrotic syndrome
- Rapidly progressive (crescentic) glomerulonephritis
- In elderly: azotemia, heart failure, and nephrotic-range proteinuria predominate
Pathology
Light Microscopy (Fig. 107-9)
Glomeruli are markedly enlarged, often filling Bowman's space. Key features:
- Diffuse endocapillary hypercellularity — proliferation of mesangial and endothelial cells
- Infiltration by monocytes and polymorphonuclear (PMN) leukocytes
- Compressed capillary lumens
- Occasional extracapillary crescents in severe cases
Immunofluorescence
- Coarse granular ("starry sky") deposits of IgG, IgM, and C3 along capillary walls
- "Hump-like" deposits
Electron Microscopy
- Large, dome-shaped, subepithelial electron-dense deposits ("humps") — pathognomonic
- Also mesangial and subendothelial deposits
Diagnosis
Serological Markers
| Test | Finding |
|---|---|
| ASO (Antistreptolysin O) | ↑ in pharyngitis (>95% positive) |
| Anti-DNase B | ↑ in skin infections (>85% positive); more sensitive for pyoderma |
| Streptozyme panel (ASO + AHT + antistreptokinase + anti-DNase) | Broad coverage |
| Serum C3 | Low in >90% of acute episodes; normalizes in 6–8 weeks |
| C4 | Usually normal (distinguishes from SLE, MPGN type II) |
- Antibody rise occurs 7–14 days after disease onset, peaks at 3–4 weeks
- A rising titer is more indicative than a single high titer
When to Biopsy
Biopsy is rarely necessary if the classic triad is present:
- Acute nephritic episode after documented strep infection
- Rising streptococcal antibody titer
- Depressed serum complement
Biopsy indications:
- Diagnostic doubt
- Complement fails to normalize by 8 weeks (consider MPGN, lupus)
- Rapidly deteriorating renal function
Differential Diagnosis (Other causes of low complement + nephritis)
| Condition | C3 | C4 | Key Distinguishing Feature |
|---|---|---|---|
| PSGN | ↓ | Normal | Post-strep latency, granular IF, humps on EM |
| MPGN Type I/III | ↓ | ↓ | Persistent low C3, double contour on LM |
| SLE nephritis | ↓ | ↓ | Anti-dsDNA, ANA, low C4 |
| Cryoglobulinemia | ↓ | ↓ | Serum cryoglobulins, hepatitis C |
| Endocarditis GN | ↓ | ↓/N | Murmur, positive blood cultures |
| IgA nephropathy | Normal | Normal | Synpharyngitic, mesangial IgA on IF |
Treatment
Active Infection
- If active streptococcal infection is still present: Benzathine penicillin G 1.2 million units IM — treats the infection and prevents spread of the nephritogenic strain
Supportive Management
| Problem | Treatment |
|---|---|
| Volume overload / edema | Loop diuretics (furosemide) + salt restriction |
| Hypertension | Antihypertensives (CCBs, ACEi in non-oliguric patients) |
| Severe oliguria/uremia | Dialysis if necessary |
There is no role for corticosteroids or immunosuppression in uncomplicated PSGN; management is purely supportive.
Prognosis
| Population | Prognosis |
|---|---|
| Children | Excellent — symptoms resolve in 2–7 days; complete recovery in >95% |
| Adults | More guarded — morbidity from pre-existing cardiovascular disease |
| Elderly | Higher risk of azotemia, volume overload, heart failure |
| ESRD | Uncommon unless comorbidities (e.g., diabetes) are present |
| Complement (C3) | Normalizes within 6–8 weeks; failure to normalize suggests alternative diagnosis |
| Hematuria | May persist as microscopic hematuria for months |
| Proteinuria | May persist for 1–2 years |
Key Memory Points
- Mechanism: Immune complex deposition → complement activation → ↓C3 (C4 normal)
- Latency: 1–2 weeks post-pharyngitis; 3–4 weeks post-impetigo
- Classic triad: Hematuria + HTN + edema (nephritic syndrome)
- Pathognomonic EM finding: Subepithelial "humps"
- Best antibody for pyoderma: Anti-DNase B (ASO often negative in skin infections)
- Normalisation: C3 normalizes by 6–8 weeks; if not → consider MPGN or lupus
- Treatment: Penicillin (if infection active) + supportive care only
Sources: Goldman-Cecil Medicine International Edition, Chapters 107 & 269; Brenner and Rector's The Kidney
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