Definition
IgA nephropathy (Berger disease) is the commonest glomerulonephritis worldwide, characterised by mesangial deposition of IgA. It shares its pathology with the renal lesion of IgA vasculitis (HSP).
Clinical presentation
- Classic: visible haematuria 1–2 days after an upper respiratory tract infection ("synpharyngitic") in a young adult
- Or asymptomatic non-visible haematuria with variable proteinuria found incidentally
- Hypertension and, over years, progressive CKD in a proportion
Investigations
- Urinalysis: haematuria (dysmorphic red cells), variable proteinuria
- Normal complement (C3) — a useful discriminator
- Renal biopsy: mesangial IgA deposition on immunofluorescence with mesangial proliferation
IgA nephropathy vs post-streptococcal GN
| Feature | IgA nephropathy | Post-streptococcal GN |
|---|---|---|
| Interval after infection | 1–2 days (URTI) | ~2 weeks (throat/skin) |
| Complement (C3) | Normal | Low |
| Typical age | Young adult | Child |
Management
- ACE inhibitors/ARBs for proteinuria and blood pressure — the mainstay
- Corticosteroids/immunosuppression for progressive disease with persistent proteinuria despite supportive therapy
- Monitor for progression
Prognosis
Markers of a worse outcome: persistent proteinuria, hypertension, and impaired renal function at presentation. Isolated haematuria with normal function generally does well.
MRCP-specific traps
- Timing separates the two post-infectious nephritides: IgA is days after a URTI; post-strep is ~2 weeks after.
- Complement is normal in IgA nephropathy (low in post-strep).
- IgA nephropathy and HSP are the same lesion in different settings.
Summary
IgA nephropathy is the commonest GN, presenting as visible haematuria 1–2 days after a URTI in young adults, with mesangial IgA and normal complement. Treat with RAS blockade, adding immunosuppression for progressive proteinuric disease. Distinguish it from post-strep GN by timing and complement.