Post-Streptococcal Glomerulonephritis (PSGN) in Children: Clinical Case Discussion & Key Learning Points
Model Case Presentation
Patient Demographics
Name: Master Arjun, Age: 8 years, Gender: Male, Informant: Mother (Reliable)
Chief Complaints
- Cola/tea-colored urine — 3 days
- Puffiness of face, especially around the eyes — 3 days
- Decreased urine output — 3 days
- Headache — 2 days
History Summary
Master Arjun was well until 3 days ago when his mother noticed his urine had turned dark, resembling cola or tea. This was associated with puffiness around the eyes, most prominent in the morning, and reduced frequency and volume of urine. He also complained of headache and mild abdominal discomfort. There is no history of facial swelling extending to the feet throughout the day (distinguishing from nephrotic syndrome), no frothy urine, and no joint pains or rash.
Importantly, 2 weeks prior to current presentation, the child had a sore throat with fever lasting 4–5 days for which he received a 3-day course of azithromycin (incomplete treatment). No history of previous similar episodes, no history of skin infections or impetigo. No family history of renal disease.
Milestones and immunization are up to date. Diet is vegetarian. No prior hospital admissions.
Examination Summary
| Parameter | Finding | Significance |
|---|---|---|
| BP | 140/95 mmHg | Hypertension (>95th percentile for age/height) |
| HR | 96/min | Mild tachycardia |
| RR | 20/min | Normal |
| Temperature | 37.2°C | Afebrile |
| Edema | Periorbital, bilateral | Fluid retention (nephritic) |
| Pallor | Mild | — |
| Cyanosis / Icterus / Clubbing | Absent | — |
| Throat | Mildly congested tonsils, no exudate | Residual pharyngitis |
Abdomen: Soft, mild bilateral loin tenderness (renal angle tenderness). No organomegaly. Mild ascites not detected clinically.
CVS: Normal heart sounds, no murmur. No raised JVP. Mild bilateral basal crepitations on respiratory examination (early pulmonary congestion due to fluid overload).
CNS: Alert and oriented. No focal neurological deficit. Fundus — no papilledema (rules out hypertensive encephalopathy at this stage).
Urine appearance: Brownish-red (hematuria).
✅ Complete Diagnosis
Acute Nephritic Syndrome secondary to Post-Streptococcal Glomerulonephritis (PSGN) — following Group A Beta-Hemolytic Streptococcal Pharyngitis — with Hypertension and Oliguria, without Hypertensive Encephalopathy.
📝 History — Exam Q&A
Post-Streptococcal Glomerulonephritis (PSGN) is the most common cause of Acute Nephritic Syndrome in children, caused by nephritogenic strains of Group A Beta-Hemolytic Streptococcus (GABHS).
The classic triad of Acute Nephritic Syndrome:
- Hematuria — smoky, cola/tea/rusty-colored urine (RBC casts on microscopy)
- Edema — periorbital (morning), then facial; not dependent
- Hypertension — due to salt and water retention
Additionally: Oliguria and mild proteinuria (non-nephrotic range, usually <2 g/day).
| Preceding Infection | Latent Period | Reason |
|---|---|---|
| Pharyngitis (throat) | 1–3 weeks (avg. 10 days) | Faster immune response to mucosal infection |
| Impetigo (skin) | 3–6 weeks (avg. 3 weeks) | Slower immune complex formation from skin; organisms differ |
💡 Mnemonic
Throat = Ten days (1–3 weeks). Skin = Six weeks (3–6 weeks).
| Source | Nephritogenic M Types | Most Common |
|---|---|---|
| Pharyngitis | M types 1, 2, 4, 12, 18, 25 | M type 12 |
| Skin (impetigo) | M types 2, 47, 49, 55, 57, 60 | M type 49 |
Skin strains differ from throat strains — there is NO overlap of immunity, hence a child who had post-pharyngitic PSGN can still develop post-impetigo PSGN.
- Most common: 5–15 years
- Peak incidence: 5–7 years
- Rare below 2 years of age
- Boys affected more than girls (2:1 ratio)
- In adults, skin infections are a more common antecedent than pharyngitis
| Feature | Nephritic (PSGN) | Nephrotic Syndrome |
|---|---|---|
| Character | Periorbital (facial), non-pitting or mildly pitting | Pitting, generalized (anasarca) |
| Timing | Most prominent in the morning; may reduce during the day | Worse in the evening; progressively worsens |
| Ascites / pleural effusion | Uncommon or mild | Common, massive |
| Mechanism | Na+ and water retention (reduced GFR) | Hypoalbuminemia (oncotic pressure ↓) |
| Proteinuria | Mild (<2 g/day, non-nephrotic) | Heavy (>3.5 g/day in adults; >40 mg/m²/hr in children) |
| Hematuria | Prominent (gross or microscopic) | Absent or minimal |
| Hypertension | Present | Usually absent (may occur) |
- Preceding sore throat or impetigo — and its timing (1–3 or 3–6 weeks ago)
- Antibiotic use — completed or incomplete course
- Character of urine: Cola, tea, rusty, smoky (hematuria) vs. frothy (proteinuria)
- Headache / vomiting / visual disturbances — features of hypertensive encephalopathy
- Breathlessness / orthopnea — pulmonary edema (hypertensive emergency)
- Urine output: Reduced (oliguria <400 mL/day or <1 mL/kg/hr in children)
- Previous episodes — rules out recurrent GN (PSGN typically does NOT recur)
- Family history: Alport syndrome, IgA nephropathy
- Joint pains, rash, oral ulcers — rules out lupus nephritis (SLE)
PSGN is an immune complex-mediated glomerulonephritis. Two main mechanisms are proposed:
- Mechanism 1 — In-situ immune complex formation: Streptococcal antigens (nephritis-associated plasmin receptor [NAPlr] and Streptococcal pyrogenic exotoxin B [SPE-B/SPEB]) deposit in the glomerulus → circulating antibodies bind to these antigens in situ → immune complex formation.
- Mechanism 2 — Circulating immune complexes: Antigen-antibody complexes form in the circulation and deposit in glomerular basement membrane.
Result: Complement activation (mainly alternate pathway) → C3 consumption → glomerular inflammation → reduced GFR → oliguria, salt-water retention → hypertension, edema, hematuria.
💡 Key Antigens
The two most studied nephritogenic antigens: NAPlr (nephritis-associated plasmin receptor — formerly called GAPDH) and SPE-B (Streptococcal pyrogenic exotoxin B / zymogen). SPE-B is considered the dominant nephritogenic antigen.
PSGN activates complement via the alternate pathway (and lectin pathway), which bypasses C1, C4, and C2.
- C3 ↓↓ — consumed via alternate pathway activation
- C4 normal — C4 is part of the classical pathway only; not consumed
- C1q normal — same reason
This pattern (low C3, normal C4) is characteristic of PSGN and helps differentiate it from Lupus nephritis (where both C3 and C4 are low — classical pathway activation).
🩺 Examination — Exam Q&A
Definition: BP ≥ 95th percentile for age, sex, and height on three separate occasions. In practice, for a school-age child: BP > 130/85 mmHg is a useful indicator, but always use age-based percentile tables.
Mechanism in PSGN: Glomerular inflammation → reduced GFR → Na+ and water retention → volume overload → hypertension. It is primarily volume-dependent (not renin-mediated). This is why the response to diuretics is good.
Features: Severe headache, vomiting, visual disturbances, confusion, seizures, altered consciousness.
Examination:
- BP measurement (severe hypertension ≥ Stage 2)
- Fundoscopy — papilledema, hemorrhages, exudates (hypertensive retinopathy)
- GCS — altered sensorium
- Focal neurological signs
- Seizures
🚨 Emergency
Hypertensive encephalopathy is a hypertensive emergency requiring IV antihypertensives (IV labetalol or sodium nitroprusside). Target: reduce MAP by no more than 25% in the first hour.
- Tachypnea, respiratory distress
- Bilateral basal crepitations (pulmonary edema)
- Raised JVP (in older children/adolescents)
- Gallop rhythm (S3)
- Periorbital and facial edema
- SpO2 may be reduced in severe pulmonary edema
In PSGN, edema is due to increased hydrostatic pressure (volume overload) with normal oncotic pressure (albumin is normal or near-normal). Fluid accumulates in loose connective tissue, which is most compliant in the periorbital area, especially when lying down at night. Hence, edema is:
- Periorbital, most prominent in the morning
- May shift to dependent areas (ankles) during the day with ambulation
- In contrast, nephrotic edema is generalized (anasarca) due to hypoalbuminemia
Renal angle (costovertebral angle) tenderness — present bilaterally due to swelling and inflammation of the kidneys (glomerulonephritis causes kidney enlargement). The kidneys themselves may be palpable in young children (normally non-palpable in school-age children). This distinguishes it from UTI, where tenderness is usually unilateral.
Subclinical PSGN refers to patients who have laboratory evidence of glomerulonephritis (microscopic hematuria, low C3, positive streptococcal serology) but no overt clinical features (no gross hematuria, no edema, no hypertension).
- For every clinical case of PSGN, there are 4–19 subclinical cases (depending on the epidemic)
- These are detected only during outbreak investigation or incidental urinalysis
- Prognosis is equally excellent
🔬 Investigations — Exam Q&A
| Test | Finding | Significance |
|---|---|---|
| Urine color | Brown/cola/smoky/rusty red | Hematuria (oxidized Hb in acid urine) |
| Dipstick | Blood +++ , Protein + to ++ | Hematuria + mild proteinuria |
| Microscopy — RBCs | Dysmorphic RBCs, >5 RBCs/HPF | Glomerular origin of hematuria (dysmorphic = glomerular) |
| Microscopy — Casts | RBC casts (pathognomonic) | Diagnostic of glomerulonephritis |
| Microscopy — WBC | May be present | Inflammatory response |
| Proteinuria (24 hr) | <2 g/day (non-nephrotic) | — |
| Specific gravity | Elevated (>1.020) | Oliguria / concentrated urine |
💡 Dysmorphic RBCs
Acanthocytes (G1 cells) — RBCs with blebs and membrane projections — are the most specific marker of glomerular hematuria. >5% acanthocytes is highly specific for GN.
| Complement | PSGN | Lupus Nephritis | IgA Nephropathy | MPGN |
|---|---|---|---|---|
| C3 | ↓↓ (Low) | ↓↓ (Low) | Normal | ↓↓ (Low) |
| C4 | Normal | ↓↓ (Low) | Normal | Normal or ↓ |
| C1q | Normal | ↓↓ (Low) | Normal | Normal |
C3 normalization: In PSGN, C3 returns to normal within 6–8 weeks.
🚨 Key Point
If C3 remains low beyond 8 weeks, rethink the diagnosis — consider MPGN (Type II / Dense Deposit Disease) or Lupus nephritis. This is a major exam question!
| Test | Antigen | Used For | Positive In |
|---|---|---|---|
| ASO (Anti-Streptolysin O) | Streptolysin O | Post-pharyngitic PSGN | ~80% of throat infections |
| Anti-DNase B (ADB) | Streptodornase B | Post-impetigo PSGN | ~90% of skin infections; also positive in throat |
| Streptozyme test | Multiple antigens | Screening (multiple antibodies) | Most streptococcal infections |
💡 Key Fact
ASO is NOT reliable for skin infections — streptolysin O is inactivated by skin lipids. Use Anti-DNase B (ADB) for post-impetigo PSGN. ADB is also the most sensitive single test for recent streptococcal infection.
Titers rise 1–3 weeks after infection, peak at 3–5 weeks, normalize over 6 months.
| Investigation | Expected Finding | Significance |
|---|---|---|
| CBC | Mild anemia (dilutional), mild leukocytosis | Volume expansion, inflammation |
| Serum Urea / BUN | Elevated | Reduced GFR (pre-renal + intrinsic AKI) |
| Serum Creatinine | Elevated (may be mild to moderate) | AKI |
| Serum Electrolytes | Hyponatremia (dilutional), hyperkalemia (if oliguric AKI) | Fluid overload, AKI |
| Serum Albumin | Normal or mildly low (dilutional) | Distinguishes from nephrotic; if very low — mixed nephrotic-nephritic |
| C3 | Markedly ↓ | Alternate pathway activation |
| C4 | Normal | Classical pathway not activated |
| ASO / ADB | Elevated (depending on site) | Evidence of prior streptococcal infection |
| Throat swab culture | GABHS may or may not be isolated (infection already treated/resolved) | Low sensitivity after antibiotic use |
| ANA / dsDNA | Negative | Excludes SLE if C4 is also low or atypical features |
Renal biopsy is NOT routinely indicated in PSGN — diagnosis is clinical. It is indicated when:
- C3 does not normalize after 8 weeks
- Features atypical for PSGN (nephrotic-range proteinuria from the start, low C4, positive ANA)
- Acute kidney injury is severe and not improving
- Age < 2 years (PSGN is rare; think other GN)
- No evidence of prior streptococcal infection
Histological findings on biopsy:
- Light microscopy (LM): Diffuse endocapillary proliferative GN — mesangial and endothelial cell proliferation, infiltration by neutrophils and monocytes ("exudative"). Glomeruli appear enlarged, hypercellular, bloodless.
- Immunofluorescence (IF): Granular deposits of IgG and C3 along the glomerular basement membrane and mesangium — "Starry sky" pattern (also described as "lumpy-bumpy").
- Electron microscopy (EM): Subepithelial humps — large, electron-dense, dome-shaped deposits on the epithelial side of the GBM (between podocytes and GBM). These are pathognomonic of PSGN.
💡 Subepithelial Humps
Subepithelial (subepithelial = between podocytes and GBM) deposits = PSGN. Compare: Subendothelial = SLE/MPGN; Intramembranous = MPGN Type II; Mesangial = IgA nephropathy.
Renal Ultrasound:
- Kidneys are bilaterally enlarged with increased echogenicity (edematous glomeruli)
- Corticomedullary differentiation preserved (helps distinguish from chronic kidney disease where kidneys are shrunken)
- Useful to exclude structural abnormalities, renal vein thrombosis
Chest X-Ray: If respiratory distress — may show pulmonary edema (bat-wing opacification), cardiomegaly.
| Feature | PSGN | IgA Nephropathy |
|---|---|---|
| Latent period | 1–3 weeks (throat); 3–6 weeks (skin) | 24–48 hours (synpharyngitic — occurs during/immediately after URTI) |
| Age | 5–15 years | Older children, adults |
| Hematuria | Gross (brown/cola-colored) | Gross (often bright red/painless) |
| Complement C3 | ↓↓ (low) | Normal |
| Serum IgA | Normal | Elevated in ~50% |
| IF | IgG + C3 (granular, starry sky) | Dominant mesangial IgA deposits |
| EM | Subepithelial humps | Mesangial deposits |
| Prognosis | Excellent (>95% recover) | Progressive in ~30-40%; may cause CKD |
| Recurrence | Does NOT recur (single episode) | Recurrent episodes of hematuria |
💊 Management — Exam Q&A
Management of PSGN is primarily supportive — there is no specific treatment to alter the glomerulonephritis itself. The disease is self-limiting in the vast majority of children.
Four pillars of supportive management:
- 1. Salt and fluid restriction — to control hypertension and edema
- 2. Diuretics — to reduce volume overload
- 3. Antihypertensives — for hypertension not controlled by diuretics alone
- 4. Eradication of streptococcus — with antibiotics (to prevent spread, not to alter GN course)
- Salt restriction: <1–2 g/day (no-added-salt diet) until edema and hypertension resolve
- Fluid restriction: Insensible loss + previous day's urine output (typically 400–500 mL/m²/day insensible) — during oliguric phase
- Potassium restriction: If hyperkalemia is present (oliguric AKI)
- Protein restriction: Mild restriction during oliguric AKI (0.5–1 g/kg/day) but maintain adequate calories; protein restriction NOT required once urine output improves
- Normal or high calorie intake — prevent catabolism
Diuretics:
- Furosemide (Loop diuretic) — first choice. Oral 1–2 mg/kg/day; IV 1 mg/kg/dose if severe edema or pulmonary edema. Works even in reduced GFR.
- Hydrochlorothiazide can be used as adjunct once edema begins to resolve.
Antihypertensives (if diuretics insufficient):
- Calcium channel blockers — Nifedipine (oral/sublingual) or Amlodipine — first-line for non-emergency hypertension
- ACE inhibitors / ARBs — use with caution; may worsen hyperkalemia in oliguric AKI; avoid until renal function stabilizes
- Hydralazine IV — for urgent hypertension in hospital
- IV Labetalol / Sodium Nitroprusside — for hypertensive emergency (encephalopathy)
🚨 ACE Inhibitors — Caution!
Avoid ACE inhibitors / ARBs in the acute oliguric phase of PSGN — they can worsen hyperkalemia and further reduce GFR. They can be used after renal function improves if proteinuria or hypertension persists.
Rationale: Antibiotics do NOT alter the course or prognosis of PSGN. However, they are given to:
- Eradicate residual streptococcal infection from the pharynx or skin
- Prevent spread of nephritogenic strains to close contacts/family members
Drug of choice:
- Penicillin V (oral) — 250 mg BD × 10 days (preferred, low resistance in GABHS)
- Amoxicillin — alternative oral option
- Benzathine Penicillin G (IM) — single dose 1.2 million units in adults; 600,000 units in children <27 kg — for compliance
- Erythromycin / Azithromycin — if penicillin allergy (note: macrolide resistance is increasing)
💡 Key Fact
Antibiotics ≠ treatment of GN. They treat/eradicate the streptococcal organism. The kidney damage from immune complexes has already been initiated by the time nephritis presents — antibiotics cannot reverse this.
- Severe hypertension (Stage 2, or symptomatic)
- Hypertensive encephalopathy (seizures, altered consciousness)
- Pulmonary edema / severe respiratory distress
- Oliguria / anuria (oliguric AKI — urine output <0.5 mL/kg/hr)
- Severe hyperkalemia (K >6 mEq/L or ECG changes)
- Severe azotemia (markedly elevated urea/creatinine)
- Inability to restrict fluids at home / poor compliance
| Complication | Features | Management |
|---|---|---|
| Hypertensive Encephalopathy | Seizures, altered consciousness, severe HTN | IV Labetalol / Sodium Nitroprusside; Benzodiazepines for seizures |
| Acute Pulmonary Edema | Tachypnea, crepitations, low SpO2 | Sit upright, O2, IV Furosemide, IV Morphine (if needed), consider dialysis if diuretic-resistant |
| Acute Kidney Injury (AKI) | Oliguria, rising creatinine, hyperkalemia, acidosis | Fluid + electrolyte management; dialysis if indications met |
| Nephrotic PSGN | Heavy proteinuria + hypoalbuminemia (rare; 5%) | May need steroids (evidence limited) |
| Rapidly Progressive GN (RPGN) | Rapidly rising creatinine, crescent formation on biopsy | IV pulse methylprednisolone ± cyclophosphamide; plasma exchange considered |
Dialysis (peritoneal dialysis or hemodialysis) is indicated if the following occur and are refractory to medical management:
- A — Metabolic Acidosis (pH <7.1) refractory to bicarbonate
- E — Electrolyte disturbances: Hyperkalemia (K >6.5 mEq/L or ECG changes)
- I — Intoxication (toxins/drugs — not relevant here)
- O — Oliguria/fluid Overload causing pulmonary edema unresponsive to diuretics
- U — Uremia (symptomatic — encephalopathy, pericarditis, BUN >100 mg/dL)
Mnemonic: AEIOU
Prognosis in children: Excellent. >95% recover completely.
| Parameter | Time to Resolution |
|---|---|
| Gross hematuria (brown urine) | 1–2 weeks |
| Hypertension and edema | 1–2 weeks |
| Oliguria (urine output normalizes) | Days to 1–2 weeks |
| C3 normalization | 6–8 weeks |
| Microscopic hematuria | Months (up to 12–18 months) |
| Proteinuria | Months (up to 6–12 months) |
Follow-up: Monthly urinalysis for 6–12 months. BP monitoring. Check C3 at 6–8 weeks. If proteinuria or hematuria persists beyond 12–18 months, or C3 does not normalize — renal biopsy.
💡 Adults vs Children
Prognosis in adults is less favorable. Adults are more likely to develop persistent proteinuria, hypertension, and long-term renal impairment (~10–40% progress to CKD in adult series). In children, this is rare (<1–5%).
PSGN is classically described as a single, non-recurring episode.
- Immunity is type-specific (directed against the specific M protein)
- Immunity to that particular M type is protective for life
- However, because different M types cause post-pharyngitic vs post-impetigo PSGN, a child can theoretically develop PSGN twice if caused by a different M type
- In practice, second clinical episodes are extremely rare
- Recurrent gross hematuria after URTI → Think IgA Nephropathy
🔭 Recent Advances — Exam Q&A
Two nephritogenic antigens have gained widespread acceptance:
- NAPlr (Nephritis-Associated Plasmin Receptor) — also known as GAPDH (Glyceraldehyde-3-phosphate dehydrogenase). It is a plasmin-binding protein; deposits in glomeruli and activates complement locally. Identified as the primary antigen in Japan/Asia-Pacific literature.
- SPE-B (Streptococcal Pyrogenic Exotoxin B) — a cysteine protease. Found in subepithelial deposits in PSGN patients. Currently considered the more dominant nephritogenic antigen in Western literature. It can activate complement directly (via alternate pathway) without antibody involvement.
Both antigens can be detected in renal biopsies of PSGN patients, supporting their role in pathogenesis.
Rarely (~1–5% of PSGN), the disease takes a rapidly progressive course:
- Rapidly worsening oliguria/anuria over days to weeks
- Rapidly rising serum creatinine (>50% increase in <3 months)
- Biopsy shows crescents in >50% of glomeruli
Management:
- IV Pulse Methylprednisolone 30 mg/kg (max 1g) on 3 alternate days → oral prednisolone taper
- Plasma exchange (plasmapheresis) — in severe cases (evidence limited in PSGN-RPGN vs ANCA-RPGN)
- Dialysis support as needed
- In adults and elderly, skin infection (impetigo/cellulitis) is more common than throat as the precipitant
- Adults with diabetes, alcohol abuse, or pre-existing renal disease have worse outcomes
- More likely to need dialysis and develop permanent renal impairment
- The classic "benign, self-limited" description applies mainly to children
- Prognosis worsens significantly with age — children >95% full recovery; adults up to 40% risk of long-term renal disease
There is currently no licensed vaccine for Group A Streptococcus. However:
- Several M-protein based vaccines are in clinical development (multivalent vaccines targeting multiple M types)
- A 30-valent M-protein vaccine (Wyeth/Pfizer) completed Phase I/II trials with good immunogenicity
- Challenges include M-protein structural diversity (>220 M types), concern for molecular mimicry leading to rheumatic fever, and limited commercial interest for developing nations
- Effective vaccination could simultaneously prevent Acute Rheumatic Fever, RHD, and PSGN — a major global health priority
PSGN is driven by complement activation. Theoretically, complement inhibition could reduce glomerular injury. Current research includes:
- Eculizumab (anti-C5 monoclonal antibody) — approved for atypical HUS and PNH; case reports of use in PSGN-related RPGN with encouraging results
- Avacopan (C5a receptor inhibitor) — approved for ANCA vasculitis; under investigation in complement-mediated GN
- These are not standard of care for PSGN currently — applicable only in severe/refractory cases
- Future: Complement inhibition may become a targeted therapy, especially for C3 glomerulopathy (which overlaps with PSGN histologically in some cases)
⚡ Key Points — Quick Revision
One-Liners for Exam
- Most common cause of Acute Nephritic Syndrome: PSGN (GABHS)
- Classic triad: Hematuria + Edema + Hypertension
- Urine color: Cola/tea/smoky/rusty brown (oxidized Hb)
- Pathognomonic cast: RBC casts (glomerulonephritis)
- Pathognomonic EM finding: Subepithelial humps
- IF pattern: Granular IgG + C3 — "Starry sky / lumpy-bumpy"
- LM: Diffuse endocapillary proliferative GN (hypercellular, bloodless glomeruli)
- Latent period — pharyngitis: 1–3 weeks; impetigo: 3–6 weeks
- Nephritogenic M type — throat: M12; skin: M49
- ASO for throat; Anti-DNase B for skin (ADB is more sensitive overall)
- Complement: C3 ↓↓, C4 Normal (alternate pathway activation)
- C3 normalizes in 6–8 weeks — if persists beyond 8 weeks → think MPGN or SLE
- Treatment: Supportive — salt/fluid restriction + furosemide + antihypertensives
- Antibiotic: Penicillin (eradicates organism, does NOT treat GN)
- ACE inhibitors: Avoid in acute oliguric phase (risk of hyperkalemia)
- Prognosis: Excellent in children (>95% full recovery)
- PSGN does NOT recur — recurrent post-URTI hematuria → think IgA nephropathy
- Biopsy indications: C3 not normal at 8 weeks, atypical features, severe AKI, age <2 years
- Eisenmenger equivalent does NOT apply — PSGN is self-limiting
- Subclinical PSGN: 4–19 subclinical cases per 1 clinical case (detected by microscopic hematuria + low C3)
🧠 Complement Patterns — Quick Comparison (Exam Favourite)
| Disease | C3 | C4 | C1q |
|---|---|---|---|
| PSGN | ↓↓ | Normal | Normal |
| SLE nephritis | ↓↓ | ↓↓ | ↓↓ |
| MPGN Type I | ↓↓ | Normal or ↓ | Normal |
| IgA nephropathy | Normal | Normal | Normal |
| HSP nephritis | Normal | Normal | Normal |
🚨 Red Flags / Don't Miss
- C3 still low at 8 weeks → Biopsy (rule out MPGN / Lupus)
- Hypertensive encephalopathy → IV antihypertensives stat
- Pulmonary edema + no urine output → Dialysis
- Nephrotic-range proteinuria from outset → Biopsy (mixed nephrotic-nephritic or another diagnosis)
- Child <2 years with nephritic picture → Always biopsy (PSGN rare; could be congenital nephrotic syndrome, SLE or other GN)