Glomerulonephritis Glomerulonephritis Michael Pakdaman MS 3 Glomerulus – Anato Histo Nephr

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Glomerulonephritis Glomerulonephritis Michael Pakdaman MS 3 Glomerulus – Anato Histo Nephr Powered By Docstoc
					Glomerulonephritis

  Michael Pakdaman
       MS - 3
Glomerulus – Anato / Histo
Nephr I / O tic ????
               Nephr I / O tic ????
   NephrOtic (PrOtein)      NephrItic (RBC +/-
   3 Systemic Diseases       casts)
    – Diabetes               3 Autoimmune
    – SLE                     – Poststrep GN (Type III)
    – Amyloidosis             – IgA Nephropathy (Type
   1 “membrane”                III)
                              – Goospasture’s (Type II)
    – Membranous GN
   2 others                 1 “membrane”
                              – Membranoproliferative
    – Minimal Change
    – Focal Segmental        2 others
                              – Crescentic
                              – Alport’s (collagen IV defect)
                Hypersensitivity
                Essentials of GN
   Type I – IgE cross-linking on presensitizes mast cells 
    inflammatory mediators released
 Type II – Antibodies directed against
  specific “enemies.” Damage cells via
  complement mediated “MAC”
  Inflammatory response NOT necessarily
  present
 Type III – Immune complex deposits (eg
  SLE)  activates complement  C5a
  chemotactic to neutrophils  damage
   Type IV – T-cell mediated
                      NephrOtic
   Membranous (#1)– Type III HS
    – Immune deposits IN the GBM
    – Assoc w/ hepatitis B antigenemia, autoimmune diseases,
      thyroiditis, malignancies, pharm (gold, penicillamine,
      captopril, NSAIDs).
   Minimal Change Disease (#1 Kids)
    – “lipoid nephrosis (why???)”
    – Tx w/ steroids
   Focal Segmental Glomerulosclerosis
    – Presents w/ acute onset; Glomerular “scarring”
    – Mutliple etiology: Podocyte injury, Nephron loss, Renal
      vasodilatation (diabetic nephropathy, sickle cell, obesity,
      Von Gierke’s, Pregnancy, Obesity, Healing of prior
      inflammatory injury)
 NephrOtic – Systemic Disease
 Diabetes  – (1) GBM thickening, (2)
  KW Nodules, (3) DIFFUSE glomerular
  sclerosis
 SLE (Type III) – SubENDOthelial
  deposits
 Amyloidosis

    “apple green”
     NephrItic – Autoimmune
 PoststrepGN (#1 acute) – type III
 (“small” – subepithelial “humps”) –
 follows sore throat or cellulitis
  – Peripheral & periorbital edema
    (autoimmune)
 IgA   – post-infectious – type III
  – Mild, self-limiting, assoc w/ Henoch-Sch
 Goodpastures    – type II
  – Men in mid 20’s
       NephrItic – Other 3
 Membranoproliferative   – MESANGIAL
  CELLS proliferate. Assoc w/ Hep C,
  SLE, a1-antitrypsin.
 Crescentic GN – Fibrin deposition in
  Bowman’s. Assoc w/ post-strep &
  membranous GN.
 Alport’s – Hereditary, type IV
  collagen defect, CN VIII defective
Membranoproliferative
  “tram-tracking”
      Linear – Type II
              Goodpasture’s
                (anti-GBM)
Capillary BM of glomerulus & alveolar walls
Granular – Type III
               IgA Nephropathy
                  (mesangial
                   deposits)
                Post-Strep GN
                (Subepithelial)
               Membranous GN
              (deposits are in the
                    GBM)
                  SLE GN
               (Subendothelial)
              Colon CA (anti-CEA
                   deposits)