ACUTE GLOMERULONEPHRITIS

Preceptor :
dr. Pulung M.Silalahi, Sp.A
Presentant :
Fatmawati (07120110091)

Department of Pediatrics
Rumah Sakit Bhayangkara
Tk.1 R.S Sukanto-Jakarta
Faculty of Medicine, Pelita
Harapan University

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) capsu

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 1-2 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 nephropathy

2. Diabetic

streptococcal species.

3. Membranous
nephropathy
4. Minimal change
disease

nephropathy
3. Henoch-Schnlein
purpura
4. Goodpasture
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
lumpy-bumpy.
On electron microscopy,
electrone dense deposurs or
humps are observed on
epithelial side of GBM.

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 immunemediated glomerulonephritis; the demonstration of
immune reactants (immunoglobulin, complement) in
glomeruli; abnormalities in serum complement; and the
finding of autoantibodies (anti-GBM) 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 cola-colored 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
. Nonspecific symptoms suchas malaise, lethargy, abdominal
pain, or flank pain are common.
. Hypertension usually normalize by 4-6 week after onset.
. Persistent microscopic hematuria can persist for 1-2 year after
the initial presentation

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-torisk 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 for a patient following acute poststreptococcal
glomerulonephritis (APSGN) primarily consists of blood pressure
measurements and urine examinations for protein and blood

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.

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