Tipe MC MIF ME Klinis

Glomerulonefritis Lesi Tidak ada kelainan Tidak ditemukan Fusi atau hilangnya foot Sindroma
Minimal (GNLM) endapan Ig atau processes sel epitel viseral nefrotik 
komplemen glomerulus. Proteinuria
selektif

The most
common cause
of the
nephrotic
syndrome in
children (peak
 2-3 years
old)

Adults may be
affected: in
some of
Hodgkin's
Disease, Non-
Hodgkin
Lymphoma
and Renal cell
carcinoma
patients
Glomerulosklerosis Fokal Sklerosis glomerulus yang Tidak ditemukan Fusi atau hilangnya foot Sindroma
Segmental (GSFS) mengenai bagian atau endapan Ig atau processes sel epitel viseral nefrotik
segmen tertentu, disertai komplemen glomerulus, tidak ada
obliterasi lumen kapiler, deposit imun kompleks
peningkatan matrix
mesangial, hialinosis
(glassy-appearing material,
resulting from insudation of
plasma proteins), hipertrofi
sel epitel, tanpa proliferasi
sel.

Nefropati IgA
(Berger’s disesase)
Mesangial and focal-
segmental proliferation and
sclerosis may be seen by
light microscopy. In bad
IgA deposited in the Mesangial and occasional Hematuria
mesangium (often with subendothelial deposits asimtomatik,
IgG, IgM, and/or C3, revealed by electron bervariasi.
but no C4, i.e., the microscopy.
alternate pathway of
cases, crescents develop. complement is being
activated.
Immunoglobulin A
nephropathy with
endocapillary proliferation
and cellular crescent
formation

Immunoglobulin A
nephropathy with
segmental sclerosis.
Membranous In this case of stage I Immunofluorescence Electron microscopy shows Sindroma
Glomerulonephritis membranous shows a finely granular uniform, evenly-spaced nefrotik
glomerulonephritis, the pattern of IgG and C3. subepithelial immune-
capillary wall is slightly These deposits soon complex deposits.
prominent and appears become incorporated
into the GBM  GBM
thickening 
("membranous“).

more rigid than normal.

However, deposits cannot
be directly visualized on
this periodic acid-Schiff
stain

The thickened capillary wall

shows numerous "holes" in
tangential sections,
indicating deposits.
(Deposits do not take up the
silver stain.) Well-
developed spikes around
the deposits are not present
in this early stage II
membranous
glomerulonephritis.
igh-power oil-immersion
view of the markedly
thickened capillary wall in
(A) stage II-III and (B) stage
III membranous
glomerulonephritis. Well-
developed spikes of
basement membrane silver-
staining material protrude
from the basement
membrane. In tangential
sections, holes are seen,
indicating the presence of
the silver-negative deposits.
In stage III, some of the
deposits are completely
surrounded by basement
membrane, and the
basement membrane
appears split in these
areas.
Glomerulonefritis Tipe 1: A pattern of Tipe 1: The immune- Tipe 2 Tipe 1: Most
Membrano-Proliferatif immune-complex disease in complex deposits are often affects
which mesangial cells irregular in size and membranoproliferative young people,
(GNMP) proliferate and send cell shape, located glomerulonephritis, type II and presents
processes between subendothelially, (also known as dense variable
Tipe 1 deposit disease) the dense
basement membrane and subepithelially, and clinical
endothelial cells. mesangially, often deposits are also found in manifestations
extending from one the basement membranes of (nephrotic
This gives the glomerular region to another, tubules syndrome,
capillary walls a "double contain IgG, C3, C4, nephritic
contour (reduplication)" or C1q, etc. syndrome,
"tram track" appearance. asymptomatic
Direct hematuria and
Tipe 2 immunofluorescence proteinuria,
shows mesangial and sometimes
capillary loop granular RPGN).
fluorescence.

Tipe 3
 Tipe 2: Light microscopy
reveals proliferation of
endothelium, thick GBM
which includes a brown
band on silver stain.

Tipe 3: Exhibits both

subepithelial and
subendothelial deposits,
together with GBM
reduplication and Tipe 2
disruption.

Rapid Progressive RPGN I Anti GBM RPGN I:

Glomerulonefritis (RPGN) disease:
immunofluorescence Goodpasture'
shows a diffuse linear s syndrome
Epithelium

Mesangium
 C’
C3a GBM
pattern of antibody RPGN II:
Chemotaxis

 Anti-GBM
Endothelium deposition along the
PMN
GBM. Severe

immune
Fibrin 
Crescent complex
disease. "Post-
infectious
RPGN" is the
severe form
RPGN III: Necrotizing of post-
and crescentic GN streptococcal
without significant or other
immune deposits bacteria-
based
glomerulonep
hritis

RPGN III:
ANCA (PMN
myeloperoxid
ase,
proteinase 3)
during the
vasculitis
syndromes