Membranous Nephropathy/Glomerulonephritis

Background/Epidemiology

• 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
  • 1/3 will go into remission
  • 1/3 will remain nephrotic
  • 1/3 will go onto develop chronic kidney disease

Aetiology

• 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

Pathophysiology

• 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

Presentation

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

Investigations

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

Management

• 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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