Synopsis
Interpret an MPGN biopsy pattern mechanistically, identify immune-complex and complement drivers, and route rare C3 disease to specialist care.
- MPGN is a light-microscopic pattern of mesangial proliferation and capillary-wall remodelling, not a single aetiological diagnosis.
- Immunofluorescence separates immunoglobulin-associated immune-complex disease from C3-dominant glomerulopathy and directs the subsequent search.
- Immune-complex MPGN prompts evaluation for chronic infection, autoimmunity, cryoglobulinaemia and monoclonal gammopathy; genuinely idiopathic disease is uncommon.
Key red flags
Oliguria, accelerating creatinine, severe hypertension or fluid overload may reflect active proliferative injury and requires urgent nephrology assessment.
Investigation priorities
Define the MPGN pattern, dominant deposits, ultrastructure and chronic damage.
Management branches
Renal histology is reported as membranoproliferative or mesangiocapillary.
- Review immunofluorescence dominance and electron-microscopy deposit location with an experienced renal pathologist.
- Map immunoglobulin-associated lesions to infection, autoimmune, cryoglobulin and monoclonal-protein pathways; map C3-dominant lesions to complement assessment.
Key medicines
ACE inhibitor or angiotensin-receptor blockerBegin and titrate one class according to the current CKD formulary, blood pressure, proteinuria, potassium and eGFR, with early laboratory review.
Disease-specific immune or complement therapyNo universal regimen is safe for an MPGN pattern. A specialist centre must select any immunosuppressive, clone-directed or complement inhibitor using the live indication, NICE decision, commissioning policy and SmPC.