A 10-year-old child is reviewed for widespread non-blanching spots over the backs of the legs. He has had crampy abdominal pain for several days and previously developed raised, itchy patches on the skin. Urinalysis shows moderate haematuria. Which histological pattern would most likely be seen if a kidney biopsy were performed?
A. Patchy basement membrane thickening
B. Normal glomerular architecture
C. Increased mesangial cellularity
D. Scattered glomerular scarring
E. Linear deposition of immunoglobulin
Correct answer: Increased mesangial cellularity (Mesangial hypercellularity)
DETAILED EXPLANATION
This child has the classic constellation of palpable purpura, colicky abdominal pain, and renal involvement (haematuria) following a minor illness — all pointing to IgA vasculitis (Henoch–Schönlein Purpura, HSP).
HSP is a small-vessel leukocytoclastic vasculitis caused by IgA immune-complex deposition, especially in the skin, gut, and kidneys.
Kidney pathology in HSP
- IgA complexes deposit in mesangium, activating complement (alternative pathway).
- This produces mesangial expansion and hypercellularity, the hallmark feature.
- Immunofluorescence shows granular IgA and C3 deposition.
Why the other options are wrong
- Linear IgG deposition → Goodpasture (anti-GBM disease).
- Normal biopsy → Minimal change disease (nephrotic syndrome), not vasculitis.
- Glomerular sclerosis → FSGS or diabetes, not associated with purpura or abdominal pain.
- Basement membrane thickening → Membranous nephropathy or Alport syndrome.
Extra MRCP-relevant points
- HSP often follows URTI, especially streptococcal infection.
- Renal prognosis is linked to degree of proteinuria and hypertension.
- Adults have worse renal outcomes than children.
- Treatment is mainly supportive, but severe nephritis may need steroids or immunosuppressants.
- Recurrences occur in one-third of cases.
CHEAT SHEET (EXAM MODE)
HSP = IgA vasculitis
- Trigger: post-infective (URTI)
- Four features:
- Palpable purpura
- Abdominal pain
- Arthralgia
- Renal disease (haematuria ± proteinuria)
Biopsy:
- Mesangial hypercellularity
- IgA + C3 granular deposits
Differentials based on biopsy patterns:
- Goodpasture → linear IgG
- Minimal change → normal LM, fusion on EM
- FSGS → segmental sclerosis
- Membranous → thickened GBM, “spike and dome”
- Alport → splitting/lamellation of GBM
Renal risk factors:
- Persistent proteinuria
- Hypertension
- Older age
Management:
- Supportive (fluids, analgesia)
- Steroids for severe abdominal pain or nephritis
- Monitor BP + urine for months
FLASHCARDS (20 CARDS)
1. What type of vasculitis is HSP?
IgA-mediated small-vessel vasculitis.
2. Typical skin finding of HSP?
Palpable purpura on buttocks and legs.
3. Common trigger for HSP?
Upper respiratory infection.
4. Key renal finding on urinalysis?
Haematuria ± proteinuria.
5. Hallmark renal biopsy feature?
Mesangial hypercellularity.
6. What deposits are seen on immunofluorescence in HSP?
IgA and C3.
7. Which complement pathway is activated?
Alternative pathway.
8. What symptom reflects gastrointestinal involvement?
Colicky abdominal pain ± GI bleeding.
9. Joint involvement finding?
Migratory arthralgia or arthritis.
10. Is HSP more common in children or adults?
Children.
11. Who has worse renal prognosis?
Adults.
12. What biopsy pattern suggests Goodpasture disease?
Linear IgG deposition.
13. Which condition shows normal biopsy on light microscopy?
Minimal change disease.
14. What biopsy pattern suggests FSGS?
Segmental sclerosis.
15. What causes basement membrane thickening?
Membranous nephropathy.
16. What feature suggests Alport syndrome?
GBM splitting (“basket-weave” pattern).
17. Is steroid therapy universally beneficial in HSP nephritis?
Evidence inconsistent; used selectively.
18. What predicts poor renal outcome?
Persistent proteinuria.
19. How often does HSP relapse?
~1/3 of cases.
20. Monitoring requirement after diagnosis?
BP and urine for at least 6–12 months.
MCQs FOR PRACTICE
1. A child presents with palpable purpura, abdominal pain, and haematuria. What is the underlying immunoglobulin involved?
A. IgG
B. IgE
C. IgA
D. IgM
Answer: C
2. Which biopsy finding is most typical of HSP nephritis?
A. GBM thickening
B. Fusion of podocyte foot processes
C. Mesangial hypercellularity
D. Linear IgG
Answer: C
3. Which factor predicts worse renal prognosis in HSP?
A. Rash severity
B. Age <10 years
C. Persistent proteinuria
D. Normal complement levels
Answer: C
4. HSP most closely overlaps with which renal disease?
A. Alport syndrome
B. IgA nephropathy
C. Post-streptococcal GN
D. FSGS
Answer: B
5. Best initial management for uncomplicated HSP?
A. Cyclophosphamide
B. High-dose steroids immediately
C. Supportive care
D. Plasmapheresis
Answer: C
SUMMARY
IgA vasculitis (Henoch–Schönlein purpura) is a small-vessel immune-complex vasculitis typically following an upper respiratory infection in children. It presents with a classic triad of palpable purpura, abdominal pain, and arthralgia, along with renal involvement such as haematuria or proteinuria. The disease results from IgA-containing immune complexes depositing in vessel walls and the renal mesangium, where they trigger inflammation through complement activation. Renal biopsy demonstrates mesangial hypercellularity with granular IgA and C3 deposition, distinguishing it from other glomerular diseases. Goodpasture syndrome instead shows linear IgG deposition, minimal change disease shows normal light microscopy, membranous nephropathy features GBM thickening, and FSGS demonstrates segmental sclerosis. Most children recover fully, but renal prognosis worsens with proteinuria, hypertension, and older age. Gastrointestinal involvement may cause severe abdominal pain or bleeding, sometimes requiring corticosteroids. Treatment is otherwise supportive, focusing on analgesia and hydration. Long-term monitoring is essential because up to one-third of patients may relapse, and progressive nephritis can occur. Although HSP overlaps with IgA nephropathy, it is distinguished by its systemic vasculitic features. Understanding biopsy patterns is key for MRCP candidates to accurately differentiate vasculitides and glomerular diseases based on clinical presentation.