Synopsis
Distinguish biopsy-proven IgA nephropathy from mimics, assess progression risk from proteinuria and eGFR trajectory, and apply contemporary supportive and specialist disease-modifying care.
- IgA nephropathy is defined by kidney-biopsy evidence of dominant or co-dominant mesangial IgA deposition in a compatible clinical setting; serum IgA is neither sensitive nor specific enough for diagnosis.
- Visible haematuria often begins during or within days of an upper-respiratory infection, unlike the longer latent interval typical of classic post-streptococcal glomerulonephritis.
- Presentation ranges from incidental microscopic haematuria to proteinuric CKD, nephrotic syndrome or rapidly progressive kidney failure, so the familiar young-adult vignette is incomplete.
Key red flags
Prolonged heavy haematuria can cause tubular obstruction and pigment injury, especially in older adults; a creatinine rise still requires exclusion of obstruction and crescentic disease.
Investigation priorities
Document haematuria, quantify albumin and total protein and identify an active glomerular sediment.
Management branches
Persistent glomerular haematuria, proteinuria or recurrent infection-associated visible haematuria raises IgA nephropathy.
- Check blood pressure, kidney trajectory, quantitative proteinuria and urine microscopy, and assess for systemic vasculitis, liver disease, infection and alternative immune disease.
- Refer according to urgency and NICE kidney criteria; discuss biopsy when results would define diagnosis, prognosis or treatment and control bleeding risk before the procedure.
Key medicines
ACE inhibitor or ARBUse one licensed agent, beginning cautiously and titrating to the highest tolerated dose with biochemical monitoring.
SGLT2 inhibitorUse the licensed once-daily CKD dose only when current NICE eligibility and eGFR criteria are met.