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Chronic Glomerulonephritis

Chronic Glomerulonephritis

Definition

  • Group of diseases with unknown etiology and unclear pathogenesis.
  • Similar clinical picture and treatment
  • Progressive evolution and predominant morphological changes in the glomeruli

Classification

Nephrotic syndrome
  • Proteinuria
  • Edema
  • Hypoproteinemia with dysproteinemia
  • Hyperlipidemia with dyslipidemia
  • Lipiduria

I. Idiopathic Nephrotic Syndrome (INS)

  • Minimal change GLN
  • Mesangioproliferative GLN with IgM deposits
  • Focal segmental glomerulosclerosis (FSGS)

II. Membraneous GLN

III. Mesangioproliferative GLN

  • With IgG deposits
  • With IgA deposits
  • With C3 deposits

IV. Membranoproliferative GLN/Mesangiocapillary

Etiology – most cases unclear

  • Bacterial infections – beta haemolytic strep; staph, meningio, pneumo, entero
  • Viral infections – flu, hep, herpes, HIV, EBV, CMV
  • Fungi – candida, histoplasma capsulatum
  • Parasites – plasmodium malariae, toxoplasma gondii
  • Drug and chemicals – volatile hydrocarbons, solvents; serums, vaccines

Pathogenesis

  • Immunocomplex
    • By circulating CIC
    • By ICs formed In situ
  • Autoimmune
    • Anti-GBM Abs, Abs against other glomerular components (podocytes, mesangial cells)
  • ICs penetrate endothelium and BM > if titre is high they form dome like shapes > proliferation of mesangial cells, decrease of capillary lumen (to encompass the deposits) > decreased BF and perfusion > decreased GFR

Idiopathic Nephrotic Syndrome (INS)

  • Common features
    • Unclear etiology and pathogenesis
    • Identical morphology – epth foot changes, mesangial proliferation, IgM deposits
    • Nephrotic syndrome
  • Minimal change GLN (lipoid nephrosis) – MC in children, no deposits
    • Pathoanat (light microscopy)
      • lack of definitive alterations in glomeruli, cellularity is normal/minimal; tubular + interstitial structures are normal
      • GBM is uniform
      • Light/absent mesangial proliferation
      • Absence of Ig deposits
      • Fusion of epth foot processes (only seen on electron microscope)
    • Clinical picture
      • Severe NS – mod/severe proteinuria (>2/3g/L); pronounced soft edema
      • Absence of arterial HTN
      • Normal renal function and serum Igs
  • Mesangioproliferative GLN with IgM deposits
    • Pathoanat – more severe morphological changes
      • Mesangial prolif with expanded mesangium
      • Deposits of IgM, C3, fibrin
      • Epithelial foot changes
    • Clinical picture
      • Nephrotic syndrome
      • Arterial HTN, hematuria, anemia
  • Focal segmental glomerulosclerosis (hyalinosis)
    • Pathoanatomy – segmental sclerosis and hyalinosis (replaces mesangial prolif)
      • Epithelial foot changes
      • Deposits of IgM, C3, fibrin
    • Clinical picture
      • Arterial HTN, hematuria
      • NS
      • Pts easily develop renal failure

Membranous GLN

  • Pathology
    • GBM changes – thickening, spikes
    • Mesangial changes – glom sclerosis, NO prolif
    • Deposits of IgG, M, A; C3, fibrin
  • Clinical picture
    • NS, HTN

Mesangioproliferative GLN – MC chronic GLN in adults

  • Patho
    • No podocyte changes or GBM changes
    • Mesangial prolif and dilation
    • Mesangial deposits of IgG, C3, fibrin
  • Morphological variants
    • With IgG and/or C3 deposits
    • With IgA deposits – disease of Berger
    • Lupus nephritis, alport syndrome
  • Clinical pic
    • NO nephrotic syndrome – proteinuria is mild <1.5g/l
    • HTN, microscopic hematuria, proteinuria, no edema
    • Best prognosis – 20 years without renal failure

Membranoproliferative GLN/Mesangiocapillary

  • Patho
    • Mesagnial and endothelial proliferation
    • Mesangial interposition, duplicated GBM
    • Mesangial deposits of C3 and IgG
  • Clinical pic
    • Nephrotic syndome, HTN, hematuria
    • Early progression to RF

Diagnosis – 4 steps

  • Enough clinical feature – proteinuria, edema, hematuria, HTN
  • Data from history and physical exam
  • Lab exam – urinalysis, serum proteins, BUN, creatinine
  • Histological verification – transcutaneous renal biopsy

Treatment

  • Etiological treatment – no value
  • Symptomatic treatment
    • Of NS – treat edema, hypoproteinemia
    • Of HTN
    • Others – pleural effusion, ascites etc
  • Pathogenetic treatment – most important
    • Drugs
      • Immunosuppressive – corticosteroids, cyclophosphamide, azathioprine, cyclosporine
      • Anticoags and antiplatelets – heparin, aspririn
      • NSAIDs – indomethacine, ibuprofen
      • Plasma separation
    • Methods
      • Conventional immunosuppresion
        • Prednisolone [1mg/kg/d for 30 days]
          • Slowly decrease by[ 5-10mg/week to reach 10-20mg/d]
        • Cyclophosphamide [0.7-1mg/kg/d]
      • Pulse treatment
        • Urbason [10-30mg/kg/d for 3 days]
          • Then continue with conventional tx
        • Cyclophosphamide [10-12mg/kg ONCE]
    • Combinations of drugs
      • Corticosteroids + anticoag
      • Corticosteroids + AC + NSAIDs
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