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The Pathology of Glomerular Diseases (IgA nephropathy (Berger's…
The Pathology of Glomerular Diseases
Minimal change disease (nil disease)
The most common cause of the nephrotic syndrome* in children (65% of nephrotic in children)
T Cell cytokines attack to the foot processes of podocytes
İdiopathic
Hypoproteinemia - Edema - Lipidemia - lipiduria (Nephrotic)
SELECTIVE PROTEINURIA
Seen in ELectron MicRoscopy
Related with Hodgkin's L. due to high cytokine level
GOOD response to steroids :D
FOcal and Segmental Lesions
Focal Segmental glomerulosclerosis (FSGS)
İdiopathic
Hyalinosis
- Sclerosing
Nephrotic
Poor Response to steroids
electron microscopy seen, might be in immunofluorescence
foot processes are damaged
Most of them will progress to chronic renal failure
HIV-associated FSGS 5%
tubuloreticular inclusions
There is a high reccurrence risk of FSGS in transplant receipents
Focal and segmental Proliferative Glomerulonephritis
Focal necrosis
The prognosis and therapy depends on the underlying disorder
IgA nephropathy (Berger's disease)
Most common serious glomerular disease
may be seen by light microscopy
Immunofluorescence shows
IgA deposited
in the
mesangium
Nephritic
Asymptomatic
Hematuria
Older age at onset, heavy proteinuria, hypertension, and presence of crescents are poor prognostic factors.
relation Henoch-Schonlein purpura
IgA deposition reccurs in 50% of transplanted kidneys.
Progress to Renal Failure 50%
DIFFUSE Glomerulonephritis
Mesengial proliferative Glomerulonephritis
Endocapillary Proliferative Glomerulonephritis
post infectious disease
prototype = post-streptococcal disease common
ACUTE and Exudative
Humps (lumpy-bumpy) on EF or IF
Obstruction of capillary lumen
H&E ; PAS POSITIVE
CHild Prognosis GOOD
ADult prognosis Less good
RELATED WITH SLE
Extracapillary proliferative Glomerulonephritis- (Crescentic GN, Rapidly progressive glomerulonephritis-RPGN)
PAS +, IF+ (except type 3), Trichrome
RPGN 2 -Immune complex glomerulonephritis
Post-infectious RPGN
severe form of post-streptococcal
RPGN 3-VASCULITIS :ANCA granulonephritis
Necrotizing and crescentic GN without significant immune deposits
Usually due to one of the systemic vasculitis syndromes
RPGN 1-Anti-GBM disease
Goodpasture's Syndrome
LUNG hemorrages
immunofluorescence shows a diffuse linear pattern of antibody deposition along the GBM.
Masugi Nephritis
20%
Membranoproliferative GN,
Lobular
pattern
Type 2
Dense deposit disease
If shows C3 no IG not like type 1
LM: brown band on silver stain.
Type 3
A very rare variant
Type 1
glomerular capillary walls a "double contour (reduplication)" or "
tram track"
appearance
This causes excessive activation of complement, low C3 levels
"C3 nephritic factor"
most common
immune complex deposition with activation of the
classical complement pathway.
is a morphologic diagnosis
, not an etiologic diagnosis.
There is high incidence of recurrence in transplant patients.
Membranous Glomerulopathy
IF shows IgG and C3
GBM thickening ("membranous“)
The most common cause of nephrotic syndrome in adults
40% recurrence after transplant
Fine granularity and Mostly nephrotic
GBM remnants form spikes
PASM
,PAS, IF, TRİCHROM +
Hereditary nephropathies
Alport disease
Nephritis
Deafness
Eye abnormality
Tubular Epithelium FOamy APPEarence
hematuria
Benign familial hematuria
idiopathic hematuria without immune deposit
Chronic Gromerulonephritis
An end-stage pool of most glomerular diseases
TUbules are lost
MAVi yerler Hyaline Sclerosis olmuş demektir
CRF