MEMBRANOUS GLOMERULONEPHRITIS

MEMBRANOUS GLOMERULONEPHRITIS
  • Characterised by diffuse thickening of glomerular capillary wall due to the subepithelial accumulation of electron dense immunoglobulin deposits
  • They can be
    • Primary (idiopathic) – 75% of cases
    • Secondary-associated with
      • Drugs –penicillamine, Captropril, gold NSAIDS
      • Malignant tumors – carcinomas of the lung and colon and melanoma
      • SLE
      • Infections- chronic hepatitis B and hepatitis C, syphilis, schistosomiasis
      • Autoimmune disorders – such as thyroiditis
Morphology
  • Light microscopy – Glomeruli either appear normal or exhibit uniform diffuse thickening of the glomerular capillary wall.
  • Electron microscopy – thickening is caused by irregular electron dense deposits containing immune complexes between basement membrane and overlying epithelial cells with effacement of podocyte foot.
  • BM material is laid down between these deposits appearing as irregular spikes protruding from the spikes.
  • These spikes are best seen by silver stains which color the BM but not deposits.
  • These spikes thickens to produce dome like protrusions and eventually close over the immune deposits, burying them within a markedly thickened irregular membrane

Reference : unckidneycenter.org/kidneyhealthlibrary/glomerular-disease/membranous-nephropathy/

  • Immunofluorescent microscopy
    • Demonstrates both immunoglobulin and complement in the deposits
    • As the disease progresses – segmental sclerosis occurs with later total sclerosis
    • Epithelial cells contain protein reabsorption droplets and there may be considerable interstitial mononuclear cell inflammation
Clinical features
  • Nephrotic syndrome – most common cause in adults
  • Proteinuria (15%)-non selective
  • Hematuria
  • Mild hypertension (15% to 35%)
Prognosis
  • Prognosis is good in women with remission and in those without nephrotic syndrome.
  • 40% of patients may have remission
  • 10% of patients die or develop renal failure in 10 years
  • 40% develop severe chronic disease or end stage renal  disease
Reference 
  1. Vinay kumar, Abul K.Abbas, Nelson Fausto, Jon C. Aster. Robbins and Cotran Pathologic basis of disease. 8th edition.
  2. Harsh mohan. Text book of Pathology.8th edition.2019
  3. Dr.A.K.Mandal, Dr. Sharmana Choudhary. Textbook of Pathology for MBBS. Vol II. Second edition 2017.