Objectives

Introduction
Definition
Epidemiolgy
Aetiolgy
Pathophysiology
Clinical features
Investigations
Treatment
Complications
INTRODUCTION
AGN is the term reserved for the variety
of renal diseases in which inflammation
of the glomerulus , manifested by
proliferation of cellular elements, is
secondary to an immunologic
mechanism.
In earlier years, AGN was known
inappropriately as Bright disease, and
almost any clinical presentation of gross
hematuria was labeled as Bright disease.
DEFINITION
Acute glomerulonephritis is a non
suppurative immune mediated
inflammatory lesion of the
glomerulus .
Is usually of sudden onset
Charaterised by accumulation of
nitrogenous waste in the blood, fluid
& electrolyte derangement
EPIDEMIOLOGY
In the tropics, children of the
preschool age are commonly
affected, while elsewhere children of
the school age are commonly
affected.
Predominantly affects children from
ages 2 to 12, average 4 to 8 year
olds.
Cont..
No racial predilection appears to
exist
The male-to-female ratio range is
1.7-2:1.
Incubation period is 2 to 3 weeks
AETIOLOGY.
Most incidents of AGN appear to be
associated with a post infectious
state.
Several bacterial and viral infections
e.g staphylococcus and
pneumonococcus, Coxsackie virus B,
Echovirus type 9, Influenza virus,
and mumps
CONT..
The most commonly recognized
clinical picture (i.e, PSAGN) follows
infection with group A beta
hemolytic streptococci.
It is also called Acute Nephritis,
Glomerulonephritis and Post-
Streptococcal Glomerulonephritis
CONT..
It may result from throat infection,
impetigo or scabietic infection with
GABHS.
Transmission:
-respiratory droplets or direct contact
with mucus secretions
-transmission via fomites is possible
but less common
PATHOPHYSIOLOGY
Most forms of AGN are mediated by an
immunologic process.
For PSAGN, the evidence suggests that
immune complexes, preformed by the
combination of specific antibodies
against streptococcal antigens, localize
on the glomerular capillary wall and
activate the complement system.
Cont..
Current evidence suggests that the
inflammatory lesion in the glomerulus is
associated with the fixation of soluble
streptococcal antigen-antibody
complexes.
Immunoglobulin G (IgG) and
complement (C3) complexes are found
on the capillary basement membrane.
The finding of C3 in the renal glomerulus
usually is associated with decreased
serum concentrations of C3 and total
hemolytic complement.
Cont..
 PSAGN can occur in epidemics but more
commonly, it is sporadic.
In patients with pharyngitis-related AGN,
the latent period is approximately 10
days, and more than 80% of patients
exhibit a significant rise in serum titer of
antistreptolysin-O (ASO).
But, a latent period is difficult to define
in patients with impetigo-related AGN,
and a rise in the titer of ASO is observed
in only 50% of patients.
Cont..
Other streptococcal indicators (eg, antihyaluronidase
[AH] titer, antideoxyribonuclease B titer [anti-DNase B])
are elevated in individuals with PSAGN secondary to
either pharyngeal or skin infections.
When a variety of antibody titers is used, almost 95% of
patients with PSAGN demonstrate evidence of a prior
streptococcal infection.
CLINICAL FEATURES
Oedema: Facial puffiness usually in the
periorbital area later it becomes more
generalized
Oliguria due to reduction in glomerular
filtration < 400ml/ day.
Hypertension; is the third cardinal
feature of PSAGN and is reported in 50-
90% of children who are hospitalized with
AGN may rage from mild to moderate.
CONT..
• Altered urine colouration:
-Gross hematuria occurs at onset in
30-50% of children
-The urine usually is described as
being smoky, cola colored, tea
colored, or rusty, dark brown or
frankly bloody
Cont..
Difficulty in breathing:
Dyspnea, orthopnea, and cough may
be present.
Pulmonary rales often are audible.
At times, the only evidence of
congestion is detected on chest
radiograph.
In the patient with an otherwise
normal cardiovascular system, cardiac
failure is unusual
Cont..
Constitutional symptoms like
malaise, lethargy, anorexia, fever,
abdominal pain, and headache.
History of the siblings and/or
household contacts of children
affected with PSAGN is important
INVESTIGATIONS
Urinalysis:
-red cell cast or granular casts
-proteinuria evidence by dip stick of +1/+2
corresponding to less than 2 g/m2/d
-specific gravity elevated
Full blood count: platelets and
Hemoglobin are decreased
Urea/creatinine –elevated
Serum protein: low
Cont..
fractionating na: is <1%in AGN,
nephrotic syndrome, dehydration unlike
ARF its >1%
renal U/S renal shows normal to slightly
enlarged kidneys bilaterally with some
evidence of increased echogenicity.
ASO titre shoulld be documented to look
for evidence of streptococcal infection in
all patients.
Cont.
 Cultures from either the pharynx or skin
may be positive.
other antibodies tests to a variety of
streptococcal antigens (eg, ASO, AH, anti-
DNase B) or to combinations of antigens
(eg, streptozyme test).
NB: a rise in the titer of the antibody,
measured at an interval of 2-3 weeks, is
more meaningful than a single
measurement.
Cont ..
C3/C4 levels help to differentiate post
streptococcal from other postinfectious forms
of AGN.
Reduced serum concentrations of C3 have
been demonstrated in 80-92% of children with
PSAGN. Values return to normal in most
children within 6-8 weeks.
The fourth component of complement (C4)
value also may be depressed; however, this is
an inconsistent finding.
Chest radiograph: pulmonary oedema
Others
Hepatitis B surface antigen
Hepatitis C antibody
Renal biopsy for selected patients
TREATMENT
Prognosis is good and mostly management
is supportive until spontaneous recovery
occurs:
Bedrest helps in maintaining adequate
blood flow to the kidney.
decreased sodium and protein intake
may be recommended in the initial phase
Fluid restrictions are adjusted according
to the patient's urinary output and body
weight.
Cont..
An accurate daily record of the patient's
weight, fluid intake and urinary output.
If residual infection is suspected,
antibiotic therapy may be needed.
Diuretics in the presence of fluid
overload.
Iron supplements for correction of
anemia
Cont..
Antihypertensives to control high blood
pressure.
GN complicating SLE or systemic
vasculitides : immunosuppression with
prednisolone, cyclophosphamide or
azathioprine may be used.
COMPLICATIONS
Pulmonary edema
Congestive Cardiac Failure
Acute Renal Failure.
Hypertensive encephalopathy
Urinary Tract Ifection
Chronic Glomerulonephritis and CRF
NB
Hypertensive encephalopathy in
approximately 5% of hospitalized children
- May be accompanied by headache, vomiting,
depressed sensorium, confusion, visual
disturbances, aphasia, memory loss, coma,
and convulsions.
-Hypertensive encephalopathy has been
reported in the occasional individual with
minimal or no edema and with minimal urinary
abnormalities.
DIFFERENTIAL DIAGNOSIS CONT.
IgA-associated glomerulonephritisEvidence
of a prior streptococcal illness usually is
lacking in individuals with HSP nephritis, and
complement values (C3 and/or C4) usually are
normal.
Henoch-Schönlein purpura (HSP) nephritis
Other IgA nephritis (Berger disease)
presents as an episode of gross hematuria
occurring during the early stages of a respiratory
illness
DIFFERENTIAL DIAGNOSIS CONT.
Others (less common)
Chronic GN (recurrence and/or relapse)
Shunt nephritis
Familial nephritis
Rapidly progressive (crescentic) GN
SLE nephritis occasionally may be confused
with PSAGN when an acute exacerbation of the
previously present nephropathy is present.
Prevention
Proper hygiene
Prompt medical assessment for
necessary antibiotic therapy should
be sought when infection is
suspected
Prophylactic immunizations
Common Causes of Gross
Hematuria
Urinary tract infection  IgA nephropathy
Meatal stenosis  Alport syndrome
(hereditary nephritis)
Perineal irritation
 Thin glomerular
Trauma basement membrane
Urolithiasis/ disease
 Postinfectious
hypercalciuria
glomerulonephritis
Coagulopathy
 Henoch-Schönlein
Tumor purpura nephritis
Glomerular  Systemic lupus
erythematosus nephritis
QUESTIONS
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