Membranous Nephropathy/Glomerulonephritis


  • Most common cause of nephrotic syndrome in adults (20-30%)
  • It can be primary (idiopathic) or secondary (usually due to other disease processes e.g. in SLE
  • It is often quoted that


  • Associated diseases/conditions include: SLE; Rheumatoid arthritis; drugs (gold- rarely used now; penicillamine; captopril); malignancy (commonly bronchus, colon, stomach, prostate, breast); Hep B; thyroid disease/diabetes mellitus (other autoimmune causes)
  • Cause unknown in idiopathic disease


  • Thought to be caused by an autoimmune reaction (type III- immunoglobulin deposition)
    • Antibodies involved are thought to be ‘M-type phospholipse A2 receptor’ (that is, in idiopathic disease)
    • Disease is characterised by diffuse thickening of the glomerular basement membrane with subepithelial ‘spikes’ on histology.  On fluoroscopy, this can be shown to be due to IgG and complement deposition


  • Nephrotic syndrome (75%)
    • Some patients will have proteinuria only; haematuria is rare; around 1/3 of patients will be hypertensive at Dx.


  • See nephrotic syndrome- definitive diagnosis is with a renal biopsy


  • Depends on symptoms/risk of progression to CKD
  • At presentation
    • If there is normal renal function (eGFR, creatinine etc) and <4g/day of proteinuria
      • Treat with ACE inhibitor +/- ARB to maintain BP <125/75mmHg and monitor the patient regularly
    • If proteinuria is (or increases to) 4-8g/day for more than 12 months
      • Cyclosporin +/- low dose steroid for at least 6 months (consider longer depending on response
  • Other treatments include cyclophosphamide and corticosteroids, rituximab and MMF.

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