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Minimal change glomerular

disease
o LM-
the glomeruli look nearly
normal

Cells of PCT laden with protein
droplets & lipid.(secondary to
tubular reabsorption of the
lipoproteins passing through the
diseased glomeruli)

o EM-
Fusion of foot processes of
visceral epithelial cells

relatively benign disorder

Accounts for about 80% of
cases of nephrotic syndrome in
children(1-7yrs) particularly in
males

Highly selective proteinuria

Management-
Corticosteroids







Focal segmental
glomerulosclerosis
o LM-
Sclerosis affects certain
segments of some but not all
glomeruli.

initially only the juxtamedullary
glomeruli (eventually all cortical
glomeruli)

Increased mesangial matrix,
obliterated capillary lumens,
and deposition of hyaline
masses (hyalinosis) and lipid
droplets

With progression- global
sclerosis with pronounced
tubular atrophy and interstitial
fibrosis

o EM-
effacement of podocyte foot
processes.

o IF-
non specific trapping of
immunoglobulins(IgM) and
complement(C3)in the areas of
hyalinosis

increasingly common cause of
nephrotic syndrome in adults
Non selective proteinuria
Management-
corticosteroids, ciclosporin
Membranous GN

o LM-
Diffuse thickening of the GCBM

Subepithelial deposits are
separated from each other by
spike like protrusions of the
basement membrane form in
reaction to the deposits.

Silver stains show a spike and
dome appearance.

o EM -
Podocytes show effacement of
foot processes

o IF-
granular deposits

a form of chronic immune
complex nephritis
Common cause for nephrotic
syndrome in adults
Proteinuria non selective
Haematuria occurs in late
stages
Management-
cyclophosphamide and
chlorambucil





Non Proliferative glomerulonephritis

Membranoproliferative GN

o LM-
Proliferation of mesangial,
epithelial and endothelial cells.

Thickening of GCBM.
The glomerular capillary wall
shows a double contour or
tram track appearance with
silver or PAS stains. Due to
cytoplasmic processes of
mesangial cells extend in to the
basement membrane of
capillaries

Capillary lumina are reduced in
size.

Glomeruli are enlarged with
accentuation of lobular
pattern.

Neutrophils and parietal
epithelial crescents
o IF-
two types recognized
Type 1 subendothelial
deposits, mainly of IgG and
early complements
components
Type 2 intramembranous
dense deposit disease
40% ESRF
Type2 worse prognosis
Management-
child-sreroid
adult- asprin&dipyradamole
Mesangioproliferative GN
IgA nephropathy
o LM-
glomeruli - normal / focal
proliferative GN,diffuse
mesangial proliferation or
(rarely) overt crescentic GN

o EM-
electron-dense deposits in the
mesangium.

o IF- mesangial deposition of IgA,
often with C3 and properdin
and smaller amounts of IgG or
IgM

Recurrent macroscopic or
microscopic haematuria
occurring within 1-2 days of a
non-specific URTI. Some
present with nephrotic
syndrome.
usually affects children and
young adults
Management-
CPP & steroids







Acute diffuse proliferative GN
(Post streptococcal GN)
LM-
Glomerulus is enlarged and
diffuse uniformly increased
cellularity of the glomerular tufts

large aggregates of immune
material (humps) in the
extracapillary area

Proliferation and swelling of
mesangial and endothelial cells

Infiltration by neutrophils and
monocytes.

Sometime necrosis of the capillary
walls

A few cases may have crescents

o EM-
Immune complexes deposited
as subendothelial,
intramembranous or often
subepithelial humps
o IF-
granular deposits of IgG and
complement within the
capillary walls and some
mesangial areas
Management-
acute phase
antihypertensives,diuretics, salt
restriction
Recovery in most
Proliferative glomerulonephritis

Crescentic (Rapidly progressive)
GN
o LM-
There is crescent formation in
most glomeruli.

Crescents are formed by
proliferation of parietal
epithelial cells and infiltration
by monocytes and
macrophages.

Occurs in response to leakage
of fibrin in to Bowman's space

o Type 1 RPGN- anti GBM
disease -20% Linear deposits
of IgG
Goodpastures syndrome
Idiopathic

o Type II RPGN- Immune
complex mediated disease -
30% Granular deposits of IgG
Post streptococcal, SLE, IgA
nephropathy, HS purpura

o Type III RPGN- pauci immune
type -50% Idiopathic
Systemic vasculitis like
polyarteritis nodosa or
Wegeners
granulomatosis



NOTE
In chronic glomerulonephritis

Kidneys are shrunken.
Finely granular surface
Loss of corticomedullary
demarcation
Arteries are prominent due to
thickened walls