RE Glomerular Pathology II: Nephritic
Terms
undefined, object
copy deck
- characteristics of Nephritic syndrome
-
hematuria
HTN
Renal insuff
Proteinuria (above 3.5 g/day=nephrotic)
immune deposits = nephritic - UA results for nephritic (in general)
-
proteinuria
"Active Urine Sediment"
-RBC cast
-dysmorphic hematuria - three mechanisms for glomerulonephritis
-
Immune complex deposits
-IgA nephropathy
-acute/diffuse proliferative
-lupus nephritis
-rapidly progressing GN
Anti-GBM (in situ imm complex)
-anti GBM GN
-Goodpastures
ANCA
-ANCA GN
-Wegeners
-microscopic polyangiitis
-Churg strauss - LM results for nephritis
-
hypercellular
mesangial
complex
focal/diffuse
segmental/global
crescentic
BM changes - IM results for GNitis
-
granular- type III (IgA, etc)
linear- type II (anti GBM)
negative- ANCA (type IV) - asymptomatic hematuria
-
Thin BM dz
Airports Syndrome
IgA nephropathy -
hematuria
LM normal
IMFL normal
EM thin BM
type IV coll dist normal -
BFH-benign familial hematuria
"thin BM dz"
excellent prognosis- no RF -
hematuria
assoc w/deafness, retinal, cornea changes
males
type IV collagen abnormal
foam cells in interstitium
basket weave BM -
Alports syndrome
chronic HTN or RF -
mesangial immune deposits
cresents can dvp
IMFL "punctate"
EM big, dark deposits in mesangials -
IgA nephropathy
viral infections may initiate or exacerbations - Henoch-Schonlein Purpura
- IgA nephropathy + vasculitis
-
hypocomplementemia
neutrophils
IMFL granular C3 on cell wall
IMFL "starry sky"
EM buffalo humps -
Acute Diffuse Proliferative GN (Post strep)
may have pos ASO
(subepithelial humps) -
LM cellular- nonspecific
IMFL "full house" staining
especially C1q (classical)
EM varies -
SLE GN
Ab's against nuclear Ag's - most aggressive lesions in SLE GN
- segmental
- activity index in SLE GN
- can treat high
- chronicity index in SLE GN
- get transplant if high
- crescent formation
-
RPGN- hallmark
-ANCA & anti GBM
(also possible in IgA nephropathy)
-proliferation of epis lining BC
-stain for fibrin
-get GBM breaks - mechanisms for RPGN
-
rapidly progressing glomerulonephritis
-anti GBM (linear IMFL)
-ANCA (neg IMFL)
-circulating immune complex (granular IMFL)
(least common cause) -
EM: crescentic GN w/ruptured capillary walls
fibrinoid necrosis
IMFL: linear IgG -
anti GBM GN
-type II is attack on type IV collagen
-if lungs involved = Goodpasture's
-young men or old females (white)
-anti GBM antibodies - anti GBM antibodies
-
anti GBM GN or Goodpasture's
in situ complex formation
young white male or old white female -
EM: crescentic GN
necrosis
IMFL: negative -
ANCA GN
medical emergency - diseases assoc'd w/ ANCA GN
-
microscopic polyangiitis (no gran or asthma, yes vasc)
Wegener's (lung granulomas, vasculitis)
Churg-Strauss (eos & asthma)
ANCA GN (no vasculitis, gran or asthma) - pathogenesis of ANCA
-
Ab's to neuts, degranulate, damage endothelium
P-ANCA
-perinuclear
-myeloperoxidase
C-ANCA
-cytoplasmic
-PR3 (proteinase)