Acute

Proliferative

Glomerulonephritis

Acute
Poststreptococca
l
Glomerulonephri
Lecture

Acute Poststreptococcal
Glomerulonephritis
Acute glomerulonephritis is a
disease characterized by the
sudden appearance of edema,
hematuria, proteinuria, and
hypertension.

APSGN
It is a representative disease of
acute nephritic syndrome in
which inflammation of the
glomerulus is manifested by
proliferation of cellular elements
secondary to an immunologic
mechanism.

Acute

Proliferative

(Poststreptococcal, Postinfectious)

Glomerulonephritis
Characterized histologically by
diffuse proliferation of glomerular
cells, associated with influx of

leukocytes.
Occurs predominantly in

males

97 percent occur in
developing countries

Acute Poststreptococcal
Glomerulonephritis
These lesions are typically caused by

immune complexes.

The inciting antigen may be

exogenous

(Postinfectious
glomerulonephritis) or

endogenous (SLE).

Acute Proliferative
Glomerulonephritis
The most common underlying
infections are

streptococc
al,
but the disorder also has

been associated with other

infections.

APSGN
It usually appears 1 to 4
weeks after a streptococcal
infection of the pharynx or skin.
It occurs most frequently in

children 6 to 10 years of age,

but adults of any age can also be
affected.

Etiology and
Pathogenesis
.
Only certain strains of group A -hemolytic
streptococci are

nephritogenic,

more than 90% of cases being traced to

types 12, 4, and 1, which can be identified
by typing of

M protein of the cell

wall.
The M and T proteins in the bacterial wall have
been used for characterizing streptococci.
Nephritogenicity is mainly restricted to certain M
protein serotypes (ie, 1, 2, 4, 12, 18, 25, 49, 55, 57,

Etiology & Pathogenesis of Ac

Prolif. G
Poststreptococcal
glomerulonephritis is an

immunologically mediated
disease.
Elevated titers of antibodies
against one or more streptococcal
antigens are present in a great
majority of patients.

Etiology & Pathogenesis of Ac

Prolif. G
Serum complement levels are low,
There are granular immune deposits
in the glomeruli, supporting an immune complexmediated mechanism.

The resulting glomerular immune complex disease

triggers complement activation and inflammation.

Pathogenesis
The 2 most widely proposed theories
include (1) glomerular trapping of
circulating immune complexes and
(2) in situ immune antigen-antibody
complex formation resulting from
antibodies reacting with either
streptococcal components deposited in
the glomerulus or with components of
the glomerulus itself, which has been
termed molecular mimicry.

Etiology & Pathogenesis

Several cationic antigens,
including a nephritis-associated
streptococcal plasmin receptor

(NAPlr),

unique to
nephritogenic strains of
streptococci, can be found in
affected glomeruli.

Etiology & Pathogenesis

Streptococcal pyogenic exotoxin
B (SpeB) and its zymogen
precursor (zSpeB), are the

antigenic
determinants in most
principal

cases of poststreptococcal
glomerulonephritis.

Morphology
Light microscopy
It shows a diffuse proliferative
glomerulonephritis with prominent
endocapillary proliferation and
numerous neutrophils.
Trichrome stain may show small
subepithelial hump-shaped deposits.
Crescent formation is uncommon and
is associated with a poor prognosis.

Light microscopic
findings

Early stage

glomerular

hypercellularity

Later stage

Proliferation

of intrinsic endothelial &

mesangial cells

Immunofluorescence
microscopy

Shows a characteristic pattern of

deposits of immunoglobulin (IgG)
and C3 distributed in a diffuse
granular pattern within the
mesangium, and glomerular
capillary walls.
Other immune reactants (eg, IgM,
IgA, fibrin, and other complement
components) may also be detected.

Electron
microscopy

The dome-shaped subepithelial electrondense deposits that are referred to as

humps.

Subendothelial immune deposits and

subsequent complement activation are
responsible for the local influx of
inflammatory cells, leading to a proliferative
glomerulonephritis, an active urine
sediment, and a variable decline in
glomerular filtration rate.
Subepithelial "humps" are responsible for
epithelial cell damage and proteinuria,
similar to that seen in membranous
nephropathy

Clinical Features Of
APG
History:

In the classic case, a

child

young

abruptly develops

malaise, fever, nausea, oliguria,

and hematuria 1 to 2 weeks after
recovery from a sore throat.

Clinical features of

Acute Proliferative

Glomerulonephritis

The patients have

red cell

casts

in the urine, mild

proteinuria (usually less than 1
gm/day), periorbital edema, and
mild to moderate

hypertension.

Clinical features of Acute

Proliferative Glomerulonephritis

In adults

the onset is
more likely to be atypical, such
as the sudden appearance of
hypertension or edema,
frequently with elevation of BUN.

Clinical features of Acute

Proliferative
Glomerulonephritis

During epidemics caused by

nephritogenic streptococcal
infections, glomerulonephritis

may be asymptomatic,
discovered only on screening for
microscopic hematuria.

Laboratory
Findings
Elevations of antistreptococcal
antibody titers and
a decline in the serum
concentration of C3 and other
components of the complement
cascade.

Prognosis
More than 95% of affected children
eventually recover totally with
conservative therapy aimed at
maintaining sodium and water
balance.
A small minority of children
(perhaps fewer than 1%) do not
improve, become severely oliguric,
and develop a rapidly progressive
form of glomerulonephritis.

Nonstreptococcal Acute
Glomerulonephritis
(Postinfectious
Glomerulonephritis)

Glomerulonephritis occurs
sporadically in association with
other infections, including
bacterial viral and parasitic.
Granular immunofluorescent
deposits and subepithelial
humps are present.