by R G 14 years ago
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Nephrotic syndrome
NephrOtic = PrOtein
Reflux Neph: Unilateral renal agenesis
Obesity
Heroin
HIV
Rapid progression to ESRD w/in months
Collapsing features
Fibrillary GN
Fibrils larger than amyloid
Amyloidosis
Causes:
Eosinophilic, Glossy material
Microscopic
Homogenous, pink
Gross
Dark brown w/ Iodine
Transplant GN
Most common cause of immune complex GN = Membranous GN
Must use IF and EM to rule out Membranous GN.
Subendothelial electron-lucent widening
Membranous GN
White
Males > Females
RARE in children
ALL glomeruli involved
Compare microscopic findings to Acute-PIGN.
Stages (I-IV) determined by EM
If immune complex deposition is stopped at early stages, changes are reversible.
Numerous, small subepithelial deposits
Finely Granular
Opposed to Coarse granular (lumpy-bumpy) in PIGN
Diffuse, thickened BM
Idiopathic FSGS
Prognosis: ESRD in 5-20 yrs
Epithelial cell detachment from BM
Focal damage of VECs
Visceral epithelial cells (Rapid Review)
Foam cells
Hyaline
Variant FSGS
Collapse of glomerular capillary loops
Obliterated capillary lumen
Segmental, Focal lesions
Juxtamedullary glomeruli
Min. Change Dz
Rx: Steroid therapy
Good prognosis (despite massive proteinuria)
Effacement of epithelial foot processes
May see mild increase in mesangial matrix
Think inflammation
NephrItic = Inflammation
GN+Lung, Type II Hypersens.
Male, Hemoptysis, Dyspnea, Discolored urine
Goodpasture's
5:1 M/F ratio
Pt develops renal failure typically?
GN, no lung
HBsAg
Classic PAN
Renal infarct
P-ANCA
Hypersensitivity angiitis (microPAN)
Crescents possible
Focal necrotizing GN
Fibrinoid necrosis
Crescents
C-ANCA
Wegener's Granulomatosis
Lung Granuloma
Henoch-Schonlein purpura
Syndrome:
Abdominal Pain
Arthralgia
Purpura
Few glomeruli, segment of glom. tuft
LN, focal prolif.
Females, 20s-40s
All Glomeruli involved
LN, diffuse prolif.
Most serious
Most common
Can also present w/
Female, 20s-40s
Subendothelial, Mesangial Deposits
"Full House"
"Full House" = Positive for the entire panel
Hyaline thrombi
Wire Loop
Normal OR
Both types are RESISTANT to STEROID THERAPY
Mesangial proliferation which advanced to the Basement membrane (HENCE MEMBRANOPROLIFERATIVE)
Alt. path of Complement
Low C3
Normal C4
MPGN-2 (DDD)
Entire BM is darkened
C3 Nephritic Factor
Mentioned in Intro. lecture as well
Immune Complex
Low C3
Low C4
MPGN-1
Subendothelial deposits
Split BM
IgG, C3
Duplicated BM
PIGN
Group A Strep (12, 4, 1, 49)
Latent period of 1-4 weeks
young>adult
male>female
Crescents possible
2 or 3 Large Humps
Coarsely granular = "lumpy bumpy"
Compare to membranous GN
Crescents may be seen
PMNs
Diffuse proliferative
5 yr survival: 100%
Dense deposit in mesangium
IgG, Complement, IgA in Mesangium
Proliferation of mesangial cells, matrix
Not to be confused with Buerger's dz (thromboangiitis obliterans)
IgA Mesangial deposits
Before Dx, rule out the following
May see IgG and C3 also.
Mesangioprolif
Normal or...
AKA Benign familial hematuria
AKA Benign idiopathic hematuria
Be cautious when making diagnosis.
There is no universally-accepted standard for normal GBM thickness
BM Thinning
Alport's
Rx: Renal transplant
EM
Multi-layer laminated
"basket-weave" appearance
IF
LM
↑ed mesangial matrix
