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@acute Nephritic Syndrome
@acute Nephritic Syndrome
SYNDROME
Clinically, presented as:
# Hematuria
# Proteinuria
# Oliguria & azotemia
# Hypertension
# Mild edema
NEPHROTIC SYNDROME
Clinically:
# Heavy proteinuria
capillary permeability
# Hypoproteinemia 2ry to loss of protein
# Generalized edema
plasma osmotic
pressurecompensatory secretion of
aldosteronesalt and water retention
# Hyperlipidemia
synthesis of lipoprotein
# Lipiduria
GBM permeability to
lipoprotein.
Causes:
# some are directly
targeting the
glomeruli(1ry glomerular
disease)
# some are due to
systemic disease that
affect glomeruli & other
tissue(2ry)
POST STREPTOCOCCAL
(ACUTE DIFFUSE
PROLIFERATIVE GN)
MINIMAL CHANGES
FOCAL SEGMENTED
GLOMERULOSCLEROSIS
MEMBRANOUS
GLOMERULONEPHRITIS
MEMBRANOPROLIFERATIVE
GLOMERULONEPHRITIS
IG A NEPHROPATHY
Common disorder
among children that
follow infection of skin
or URT by nephritogenic
strain of B-haem.
streptococci.
Main cause of NS
among children
< 15 years
INCIDENCE
Most frequent cause of
NS among adults in
western countries
Normal looking
glomeruli with LM &
diffuse loss of
epithelial foot
processes by EM.
Deposition of immune
complex formed
predominantly of Ig A
-immune complex
deposited within the
glomeruli initiate
inflammation by
activation of
complement system
-might be 1ry
epithelial injury(no
immune complex
deposition)
-disorder in Tlymphocytes leading
to elaboration of
cytokines that affect
synthesis of
nephrin.
Consequently, there
is loss of podocyte.
1.nephritic syndrome
2.low serum
complement level
3.high titre of antistreptolysin O(ASO) in
serum
In NS, there is
neither
hypertension nor
hematuria
Good prognosis
with excellent
response to
corticosteroid
therapy in > 90% of
affected children &
less figures in adult.
PATHOGENESIS
-injury to epithelial cell
Immune complex
lead to focal
mediated disease:
hyperpermeable foci
-1ry: due to in situ
entrapment of plasma
deposition of immune
protein & lipid
complexes against renal
-result in mesangial cell
autoantigen
reaction with mesangial -2ry: due to circulating
matrix
immune complexes
against exogenous
antigen
1.non selective
proteinuria
2.may progress to NS
3.may develop
hypertension &
hematuria
CLINICAL PICTURES
NS, sometimes nonnephrotic range nonselective proteinuria
-genetic or aquired
abnormality of immune
regulation leading to
mucosal Ig A synthesis in
response to resp of GIT
exposure to environmental
agents. Ig A and Ig A
complex then get trapped
within mesangium,
activate alternate
complement pathway &
initiate glomerular injury.
-Diffuse in mesangial
cells with infiltration by
neutrophils leading to
compression of capillary
lumina (bloodless
glomeruli)
-cresent
formation(proliferation
of parietal cells)
Normal looking
glomeruli
Granular deposits of Ig G
and C3 along capillary
wall
No deposits
Scattered subepithelial
deposits shaped like
humps
Diffuse loss of
epithelial foot
processes
MICROSCOPIC PICTURES
LIGHT MICROSCOPE
Some show segmental
Diffuse thickening of
obliteration of capillary
GBM, normal glomerular
loop with mesangial
cellularity.
matrix, collapsed GBM &
accumulation of lipid &
proteinaceous material.
Usually negative
FLUOROSCENCE MICROSCOPE
Typical granular deposits
of Ig & complement
along GBM
ELECTRON MICROSCOPE
Focal segmental in
Subepithelial deposits
mesangial matrix with
nestle against GBM &
prominent injury of
separated from each
overlying podocyte
other by small spike-like
protrusion of GBM
matrix