Nephritic and nephrotic syndrome in pediatrics
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pediatric nephritic syndrome causes clinical features laboratory findings management
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pediatric nephrotic syndrome minimal change disease features diagnosis treatment complications
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Nephritic vs Nephrotic syndrome in pediatrics
| Feature | Nephritic syndrome | Nephrotic syndrome |
|---|---|---|
| Core problem | Glomerular inflammation | Increased glomerular permeability to protein |
| Urine findings | Hematuria (often cola/tea-colored), RBC casts, mild-moderate proteinuria | Heavy proteinuria (nephrotic range), lipiduria/fatty casts, usually little/no gross hematuria |
| Edema | Mild to moderate (often periorbital) | Marked generalized edema (anasarca), ascites possible |
| BP | Often high | Usually normal or mildly elevated |
| Kidney function | May have reduced GFR, ↑Cr, oliguria | Often preserved initially |
| Serum albumin | Mildly low or normal | Low (hypoalbuminemia) |
| Lipids | Usually not strikingly high | Hyperlipidemia common |
| Typical pediatric causes | Post-streptococcal GN, IgA nephropathy, lupus nephritis, membranoproliferative patterns, rapidly progressive GN | Minimal change disease (most common in children), FSGS, membranous (less common), congenital nephrotic syndromes |
Pediatric nephritic syndrome: key points
- Typical triad: hematuria + edema + hypertension, with variable AKI.
- Often follows infection (eg, post-strep GN) after latent period.
- Labs commonly include:
- Urinalysis: dysmorphic RBCs, RBC casts, subnephrotic proteinuria
- Complement (C3/C4) may help etiology (eg, low C3 in PSGN)
- Renal function, electrolytes, ASO/anti-DNase B when indicated
- Management is cause-directed plus supportive:
- Salt/fluid restriction, loop diuretics
- BP control
- Treat underlying trigger
- Urgent nephrology review if severe HTN, rising creatinine, oliguria, or suspected RPGN
Pediatric nephrotic syndrome: key points
- Defined by:
- Nephrotic-range proteinuria
- Hypoalbuminemia
- Edema
- Hyperlipidemia (supportive feature)
- In children, minimal change disease (MCD) is the leading cause (about 70 to 90% in childhood; Harrison’s).
- Typical first presentation: periorbital edema progressing to dependent/generalized edema.
- Initial treatment (steroid-sensitive idiopathic cases):
- Prednisone/prednisolone regimen per pediatric protocol
- Salt restriction, edema management
- Vaccination/infection prevention counseling
- Important complications:
- Serious infections (eg, spontaneous bacterial peritonitis)
- Thrombosis risk
- Hypovolemia/AKI in overdiuresis or severe intravascular depletion
When to suspect something other than simple steroid-sensitive nephrotic syndrome
Red flags for secondary or non-MCD disease:
- Persistent gross hematuria
- Sustained hypertension
- Low complement
- Impaired renal function at presentation
- Age <1 year or older child/adolescent atypical pattern
- Poor steroid response
These children usually need broader workup and often kidney biopsy.
Practical exam/ward memory aid
- Nephritic = blood + pressure + inflammation
- Nephrotic = protein + puffiness + low albumin
Source used:
- Harrison’s Principles of Internal Medicine, 21e: nephritic syndrome clinical pattern (p. 8568) and minimal change disease epidemiology in childhood nephrotic syndrome (p. 8592).
Detail notes on individual disease
Detailed notes on individual pediatric glomerular diseases
1) Post-streptococcal glomerulonephritis (PSGN)
Category: Nephritic
- Typical age: 5 to 12 years
- Trigger: 1 to 3 weeks after streptococcal pharyngitis or skin infection
- Pathogenesis: Immune complex mediated glomerular inflammation
- Clinical
- Cola/tea-colored urine
- Periorbital edema
- Hypertension
- Oliguria (variable)
- Labs
- Hematuria with RBC casts
- Mild-moderate proteinuria
- Low C3 (usually returns to normal in 6 to 8 weeks)
- Elevated ASO/anti-DNase B (depending on site of infection)
- Management
- Supportive: salt/fluid restriction, diuretics, BP control
- Treat active streptococcal infection if present
- Prognosis: Excellent in most children, full recovery common
2) IgA nephropathy (Berger disease)
Category: Mostly nephritic (can have mixed picture)
- Typical clue: Gross hematuria occurring during or within 1 to 2 days of URI (synpharyngitic)
- Pathogenesis: Mesangial IgA deposition
- Clinical
- Recurrent episodic hematuria
- Microscopic hematuria between episodes
- Variable proteinuria
- Labs
- Usually normal complement
- UA with hematuria ± proteinuria
- Diagnosis: Definitive by kidney biopsy (IgA-dominant mesangial deposits)
- Management
- BP/proteinuria control (ACEi/ARB when indicated)
- Immunosuppression in selected higher-risk cases
- Prognosis: Variable, many mild cases but some progress over years
3) Henoch-Schonlein purpura nephritis (IgA vasculitis nephritis)
Category: Nephritic/nephritic-nephrotic overlap
- Systemic features: Palpable purpura, arthralgia, abdominal pain
- Renal spectrum: Microscopic hematuria to nephritic syndrome to nephrotic-range proteinuria
- Labs: Similar renal findings to IgA nephropathy; complement usually normal
- Management
- Mild renal disease: monitoring and supportive care
- Significant proteinuria, nephritic syndrome, or declining renal function: nephrology-directed immunosuppression
- Prognosis: Good in most, depends on renal severity
4) Lupus nephritis (pediatric SLE)
Category: Can be nephritic, nephrotic, or mixed
- Clues: Multisystem SLE signs (rash, arthritis, cytopenias, serositis)
- Labs
- Hematuria/proteinuria
- Low C3/C4
- Positive ANA, anti-dsDNA
- Diagnosis: Kidney biopsy classifies nephritis (ISN/RPS classes) and guides therapy
- Management
- Steroids + steroid-sparing immunosuppressants (MMF/cyclophosphamide etc by class)
- BP/proteinuria control, renal-protective strategy
- Prognosis: Improved with modern therapy, but relapses and CKD risk exist
5) Rapidly progressive glomerulonephritis (RPGN, crescentic GN)
Category: Severe nephritic emergency
- Pattern: Rapid creatinine rise over days to weeks, active urinary sediment
- Etiologies: Immune complex, anti-GBM, ANCA-associated vasculitis
- Clinical: AKI, edema, HTN, sometimes systemic vasculitis signs
- Workup: Urgent serologies + biopsy
- Management: Urgent nephrology care, high-dose steroids ± cyclophosphamide/rituximab, sometimes plasmapheresis (cause-specific)
- Prognosis: Time-sensitive, delay worsens renal outcome
6) Minimal change disease (MCD)
Category: Nephrotic (most common pediatric cause)
- Typical age: 2 to 8 years
- Clinical
- Sudden periorbital edema progressing to generalized edema
- Often normal BP and preserved renal function
- Labs
- Heavy proteinuria
- Hypoalbuminemia, hyperlipidemia
- Usually no gross hematuria
- Pathology: Normal LM, podocyte foot process effacement on EM
- Management
- First-line corticosteroids (usually steroid-sensitive)
- Edema management, salt restriction
- Course: Relapses common, long-term kidney failure uncommon in steroid-sensitive cases
7) Focal segmental glomerulosclerosis (FSGS)
Category: Nephrotic (often steroid-resistant)
- Clinical clues
- Nephrotic syndrome with hematuria/HTN more common than MCD
- Higher chance of reduced GFR
- Etiology: Primary or secondary (obesity, reflux nephropathy, reduced nephron mass, genetic forms)
- Diagnosis: Biopsy (segmental sclerosis in some glomeruli)
- Management
- Steroid trial in selected cases
- Calcineurin inhibitors often used in resistant disease
- RAAS blockade for proteinuria
- Prognosis: Higher CKD progression risk than MCD
8) Membranoproliferative pattern / C3 glomerulopathy
Category: Often nephritic-nephrotic mixed
- Mechanism: Immune complex or alternative complement pathway dysregulation
- Clinical: Hematuria + proteinuria, HTN, reduced kidney function possible
- Labs: Persistent hypocomplementemia (often C3)
- Diagnosis: Biopsy with IF/EM patterns, complement pathway evaluation
- Management: Cause/mechanism specific, nephrology-led; BP/proteinuria control essential
- Prognosis: Variable, can be progressive
9) Congenital nephrotic syndrome
Category: Nephrotic (infancy)
- Onset: First 3 months of life
- Causes: Often genetic (NPHS1, NPHS2, WT1 and others)
- Clinical: Severe edema, heavy protein losses, failure to thrive, infections/thrombosis risk
- Management
- Intensive nutritional and albumin support
- RAAS modulation where possible
- Often progresses to need dialysis/transplant planning
- Prognosis: Depends on subtype, generally severe without definitive renal replacement strategy
10) Secondary nephrotic syndromes in children
- Infections: Hepatitis B/C, HIV (region/context dependent)
- Systemic disease: SLE
- Drugs: NSAIDs and others (less common in pediatrics than adults)
- Approach: Treat underlying cause + nephrotic care + nephrology follow-up
Biopsy indications in a child with glomerular syndrome (high-yield)
Consider early biopsy when atypical features are present:
- Age <1 year
- Macroscopic persistent hematuria with nephrotic syndrome
- Sustained hypertension
- Low complement beyond expected recovery window
- Impaired kidney function at presentation
- Steroid resistance/frequent atypical relapses
- Systemic disease suspicion (SLE, vasculitis)
Quick one-line differentiation of major pediatric entities
- PSGN: Post-infectious nephritic + low C3, usually self-limited
- IgA nephropathy: Recurrent hematuria with URI, complement usually normal
- Lupus nephritis: Multisystem autoimmune + low complements + biopsy class guides therapy
- MCD: Most common pediatric nephrotic, steroid responsive
- FSGS: More severe nephrotic, more steroid resistance, higher CKD risk
If you want, I can turn this into:
- an exam revision sheet (one page),
- a bedside workup algorithm, or
- a steroid-sensitive vs steroid-resistant nephrotic syndrome flowchart.
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