28/04/2013 by admin | Renal
  1. Types of presentation:
    1. o Acute/chronic renal failure
    2. o Nephrotic syndrome (=oedema, proteinuria, hypoalbuminaemia)
    3. o Haematuria
    4. o Proteinuria and HTN
  2. Cardinal signs of GN are: proteinuria, haematuria, urinary cysts.
  3. GN affects both kidneys symmetrically
  4. GN may affect kidneys only = primary GN or be systemic = Wegeners granulomatosis/SLE/other secondary glomerulonephritides.
  5. Ix: biopsy (=light microscopy, immunoflourescenes, electron microscopy).
    1. o There are many different histological sub-types of GN – these can be considered as follows…
  1. Types of acute GN:
    1. o Acute renal failure = (‘rapidly progressive GN’ = RPGN): characterised by presence of crescents (crescentric-shaped proliferation of cells in Bowmans capsule). Most commonly seen in GN linked to vascultic disease (=Wegerners, Goodpastures syndrome [acute renal failure and pulmonary haemorrhage cuased by circulating anti-glomerular basement membrane antibody], and post-streptococcal infection GN). Time is of the essence and patients can go from normal renal functiondialysis in few weeks if not managed quickly.
    2. o Nephrotic syndrome: light microscopy shows thickened basement membranes due to numerous sub-epithelial immune complex deposits if IgG and complement C3. Usually idiopathic. Underlying malignancy seen in 10%. Can rarely relate to SLE, RA. May have a renal vein thrombosis and present with PE (due to hypercoagulability). In minimal change GN – podocyte foot process are fused on electron microscopy. Focal segmental glmoerulosclerosis (FSGS) is similar except glomeruli have segmental sclerotic lesions.
    3. o Incidental haematuria and/or proteinuria: often due to IgA nephropathy (=Berger’s disease). p/c – marked haematuria after URTI. On histology = mesangial deposition of IgA with variable segmental mesangial proliferation. 20-40% progress to renal failure. IgA nephropathy can also occur in long-standing alcohol abuse with liver disease.
    4. o Chronic GN: small, shrunken kidneys on USS and chronic fibrotic changes and glomerulsclerosis on biopsy. If previous history of proteinuria/haematuria – assume GN disease. Rarely responds to Tx.
  2. Ix of GN:
    1. o Assess renal function (=serum creatinine, creatinine clearance, urine dipstick, microscopy for RBCs, and ‘urinary casts’, 24h urinary protein extraction and USS for renal size).
    2. o If >1g/d proteinuria = GN
    3. o cANCA +ve = Wegeners granulomatosis
    4. o ANF/C3/C4 +ve = SLE
    5. o Anti-glomerular basement membrane (anti-GBM) +ve = Goodpastures
    6. o Anti-streptolysin O (ASO) +ve = post-streptococcal GN
  3. Tx:
    1. o Minimal change GN = corticosteroids (create remission – 50% relapse). If not effective, consider aggressive immunosuppression
    2. o Membraneous GN = steroids and chlorambucil (ponticelli regimen). If GN is drug induced – stop causative agent.
    3. o RPGN/secondary GN = aggressive immunosuppression (=corticosteroids, cyclophosphamide, plasmaphoresis) 
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