ACUTE

GLOMERULONEPHRITIS
Preceptor :
dr. Pulung M.Silalahi, Sp.A
Presentant :
A. Deza Farista (1102011001)
Department of Pediatrics
Rumah Sakit Bhayangkara
Tk.1 R.S Sukanto-Jakarta
Faculty of Medicine,
Universitas Yarsi

INTRODUCTION
Glomerulonephritis is a term used for kidney diseases with
an inflammation and proliferation of glomerular cell.
Glomerulonephritis (GN) is generallycategorizedinto either
proliferative or non-proliferative .
Diagnosing the pattern of GN is important because outcome
& treatment depend on the type.
Acute post streptococcal glomerulonephritis is the most
common cause glomerulonephritis in children.
Acute glomerulonephritis usually recognize based on clinical
appearance such as gross hematuria, fluid overload that
manifested as edema and hypertension, and some finding
of insufficiency kidney function like increasing of BUN and
creatinine.

1. ANATOMY

BLOOD SUPPLY OF THE KIDNEY

Renal artery
Segmental Arteries
Interlobar Arteries
Arcuata arteries
Interlobular Arteries
Afferent arterioles
Glomerular cappilaries
Efferent arterioles
Peritubular capillaries
Interlobular veins
Arcuate veins
Interlobar veins
Renal vein

THE NEPHRON
Consist of two parts :
1. Renal corpuscle
- glomerulus
- glomerular
( Bowmans) capsul
2.

Renal tubule
- proximal convuluted

tubule
- loop of henle
- distal convuluted
tubule

2. PHYSIOLOGY
The kidney do major work of the urinary system. The other
parts of the system mainly passageaways and storage areas.
Function of kidney include :

Regulation of blood ionic composition.

Regulation of blood pH.

Regulation of blood volume.
Regulation of blood pressure.
Maintenence of blood osmolarity.
Production of hormones.
Regulation of blood glucose level.
Excretion of wastes and foreign substances. By forming
urine, kidneys help excrete waste.

URINE FORMATION
1. Glomerular filtration : water and most
solutes in blood plasma move across the
wall of glomelural capillaries into the
glomerular capsule then into renal tubule.
2. Tubular reabsorbtion :water and
solutes return to the blood as it flows
through peritubular capillaries and vasa
recta.
3. Tubular secretion. : fluid flows along
the renal tubule and through the collecting
duct, the tubule and duct cells secrete other
materials, such as wastes, drugs,and excess
ions, into the fluid.

GLOMERULAR FILTRATION
Glomerular

capillaries

are

relatively impermeable to proteins.

The fluid that enters the capsular
space is called glomerular filtrate.
More

than

99%

of

glomerular

filtrate return to the blood stream

via tubular reabsorbtion, so only 12 liters is excreted in to urine.

 The glomerular capillay wall is the filtration unit and

consist of the following structures :
1. Endothelial cells
2.Glomerular basement membrane (GBM)
3. Podocytes

 Mathematically,
the
GFR
equals the product of Kf and
the net filtration pressure:
GFR = Kf \ Net filtration
pressure
The net filtration pressure
represents the sum of the
hydrostatic
and
colloid
osmotic forces that either
favor or oppose filtration
across
the
glomerular
capillaries.
The GFR can therefore be
expressed as GFR = Kf \ (PG
PB pG + pB)

Definition
Glomerulonephritis
is
an
inflammatory
process affecting primarily the part of kidney
that filters blood called glomerulus, with
infiltration
and
proliferation
of
acute
inflammatory cells.
The inflammation happens because of an
immunologic process that makes pathologic
abnormality of glomerulus
There can be both acute glomerulonephritis
and chronic glomerulonephritis

Acute Glomerulnephritis

Acute
glomerulonephritis
is
a
disease
characterized by sudden appearance of :
1. Edema
2. Hematuria
Nephritic Syndrome
3. Hypertension
4. Oliguria
This due to the immunologic response which
triggers inflammation and proliferation of
glomerular tissue that result in damage to the
glomerular layer.

EPIDEMIOLOGY
PSAGN can happened either sproradically or epidemically
Epidemic outbreaks have taken place in communities with
densely populated dwellings that have poor hygienic
conditions.
Sporadic APSGN following upper respiratory tract infection is
more common in winter and spring in temperate areas,
whereas skin infections are commonly found to precede
APSGN in the more tropical and subtropical areas.
In developing countries APSGN, usually occurs in children,
predominately males, most cases occur in patients aged 5-15
years.

NON INFECTIOUS

Primary renal disease

INFECTIOUS

Systemic disease
1. Bakteri :

1. MPGN

1. Lupus nephritid

most common :

2. IgA

2. Diabetic

streptococcal species.

nephropathy
3. Membranous
nephropathy
4. Minimal

nephropathy
3. HenochSchnlein
purpura

change

4. Goodpasture

disease

syndrome

2. Virus
3. Fungal
4. Parasites

PATHOLOGY
Glomerular lesion in
acute GN result in
glomerular deposition
of immune complexes.
On gross appearance
the kidneys appear
symmetrically
enlarged.
Immunoflueressence
microscopy reveals a
pattern of lumpybumpy.
On electron
microscopy, electrone
dense deposurs or
humps are observed

PATHOGENESIS
Glomerular injury may be result of : genetic,
immunologic , perfusion, or coagulation disorder.
Immunologic injury to the glomerulus results in
glomerulonephritis .
Evidence that glomerulonephritis is caused by
immunologic
injury
includes
morphologic
and
immunopathologic
similarities
to
experimental
immune-mediated
glomerulonephritis;
the
demonstration of immune reactants (immunoglobulin,
complement) in glomeruli; abnormalities in serum
complement; and the finding of autoantibodies (antiGBM) in some of these diseases .

PATHOGENESIS
Two
major
mechanism
of
immunologic
associated injury
have been established :
1. injury resulting from deposition of
soluble circulating antigen-antibody
complexes in the glomerulus.
2. Injury by antibodies reacting in
situ within glomerulus

PATHOGENESIS IN PSAGN
(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.

 Host factor
Streptococcus factor
- Nephritogenic strains of group A
beta-hemolytic streptococci.
- M Protein in bacterial wall (M
protein serotypes ie, 1, 2, 4, 12, 18,
25, 49, 55, 57, and 60)
- Nephritogenic antigen : Nephritis
associated streptococcal plasmin
receptor (NAPLr) and pyogenic
exotoxin ( SPEB)

Clinical Manifestation
Typical presentations

Atypical presentation

1. Hematuria: the classic description of tea- or colacolored urine occurs in approximately 2560% of
patients
2. Edema: Edema usually appears abruptly and first
involves the periorbital area, but it may be
generalized
3. Hypertension
:
Hypertension
occurs
in
approximately 8090% of cases . Cerebral
complications of hypertension including headaches,
seizures, mental status changes, and visual changes
occur in 3035% of children
4. Nonspecific symptoms suchas malaise, lethargy,
abdominal pain, or flank pain are common.

1. Latent Phase:
The interval between exposure to
an infectious organism and the
clinical appearance of disease.
2. Acute Phase
The acute phase generally
resolves within 6-8 week.
3. Recovery Phase
Recovery phase occurs after
resolution of fluid overload with
diuresos-either spontaneous
and/or pharmacologically
induced- along with normalization
of blood pressure and resolution
of gross hematuria.

DIAGNOSIS
Anamnesis
Physical examination
Laboratory findings
1. urinalysis : RBC casts, proteinuria, PMN
leukocytes
2. GFR is often decreased during acute
phase of the disease
3. Serological markers : ASO titer and
depression of c3 level.
Renal biopsy

DIFFERENTIAL DIAGNOSIS

COMPLICATION
Hypertensive encephalopathy.
Prolonged hypertension can lead
to intracranial bleeding.
Other potential complications
include heart failure,
hyperkalemia,
hyperphosphatemia,
hypocalcemia, acidosis,seizures,
and uremia.
Acute renal failure

PREVENTION

Vaccine ?
The most effective public health
measure in the developing world is to
improve hygiene and provide better
housing conditions to avoid
overcrowding.

MANAGEMENT AND
TREATMENT
Treatment remains largely supportive and usually
addresses the most urgen problem hypertension.
The importance of supportive therapies in acute
glomerulonephritis can not be over emphasised. Tight
blood pressure control, appropriate use of diuretics,
and control hyperkalemia, uraemia, and fluid overload,
if necessary by dialysis, are quite literally life saving.
In most cases of post-streptococcal glomerulonephritis
where inflammation does resolve spontaneously,
supportive therapies alone will be sufficient with
improved renal function being seen between four and
14 days after the initial acute failure in 95% of patient.

1. Supportive treatment

Blood pressure control

Dialysis
Antibiotic
Immunosupression

1. Diet and Activity

2. Inpatient Management
3. Long Term Monitoring

1. Diet and activity

A low-sodium, low-protein diet should be prescribed during the
acute phase, when edema and hypertension are in evidence.
Limitation of fluid and salt intake is recommended in the child
who has either oliguria or edema.

Potassium

intake

should

be

restricted

to

prevent

hyperkalemia.
Limited activity is probably indicated during the early phase of
the disease, particularly if hypertension is present. Bedrest
may lessen the degree and duration of gross hematuria if
present.

2. In Patient Management
Hospitalization is indicated if the child has significant hypertension
or a combination of oliguria, generalized edema, and elevation of
serum creatinine or potassium.
Severe Hypertension

Severe hypertension, or that associated with signs of cerebral

dysfunction, demands immediate attention. Three drugs are
commonly cited as having a high benefit-to-risk ratio:
1. Labetalol (0.5-2 mg/kg/h intravenously [IV]),
2. Diazoxide, and
3. Adnitroprusside (0.5-2 mcg/kg/min IV)
Severe hypertension without encephalopathy
1. hydralazine or nifedipin

Mild-to-moderate hypertension
1. bedrest, fluid restriction.
2. The use of loop diuretics, such as furosemide (1-3 mg/kg/d oral [PO],
administered 1-2 times daily), may hasten resolution of the hypertension.
Edema
1. Restriction of fluids
2. Loop diuretics (furosemide).
3. If congestion is marked, administer furosemide parenterally (2 mg/kg).
Anuria or oliguria
Because they may be ototoxic, avoid large doses of furosemide in children
with symptoms of anuria or severe and persistent oliguria. In addition,
osmotic diuretics, such as mannitol, are contraindicated, as they might
increase vascular volume.

3. Long-Term Monitoring

Long-term

follow-up

poststreptococcal
consists

of

blood

for

patient

glomerulonephritis
pressure

following
(APSGN)

measurements

examinations for protein and blood

acute

primarily
and

urine

PROGNOSIS
Complete recovery occurs in >95%
of children with APSGN.
Recurrences are extremely rare.
Mortality in the acute stage can be
avoided by appropriate management
of acute renal failure, cardiac failure,
and hypertension.

THANKYOU