Acute glomerulonephritis(AGN)

Teacher ： Yanli Zhang

Department ： the Third hospital
affiliated to ZhengZhou University
 OUTLINE
Introduction Laboratory
Etiology and evaluation
epidemiology Diagnosis
Pathogenesis Treatment
Pathology  Prognosis
Clinical Prevention
manifestations
 1 Introduction
The disease is the classic example
of the acute nephritic syndrome:
the sudden onset of gross
hematuria , edema, hypertension,
and renal insufficiency

It was the most common cause of

gross hematueria in children; now
is IgA nephropathy
 Introduction
The course of AGN is less than 1 year
Most AGN belong to acute
poststreptococcal glomerulonephritis
(APSGN)
AGN is 53.7% of urine system diseases
during same time
AGN is common during 5~14 years old
Male: female is equal to 2:1
 2 Etiology and epidemiology

APSGN follows infection of throat or skin

During cold weather, APSGN follows
streptococcal pharyngitis ,whereas
during warm weather ,APSGN follows
streptococcal skin infections or
pyoderma
The disease is most commonly sporadic
 3.Pathogenesis
Although morphologic studies and a
depression in the serum complement
(C3) level strongly suggest that APSGN
is mediated by immune complexes, the
precise mechanisms by which
nephritogenic streptococci induce
complex formation remain to be
determined.
 pathogenesis
Formation of immune complexes
including antibodies and streptococcal
antigens
Localization (deposition) on
subepithelial portion of glomerular
basement membrane
This leads to localized mesangial and
endothelial cell proliferation
 Streptococci infection
complex formation

C3↓
AGN

Mesangial cell
proliferation Mesangial matrix
Blood capillary close off
destroy

GFR↓ Oliguria or anuira Proteinuria

hematuria
Salt and water Edema
retention hypertension
 4. Pathology
Most forms of AGN, the kidney appear
symmetrically enlarged .
On early phase , classic AGN appear
endocapillary proliferative
On light microscopy, AGN appear
enlarged and relatively bloodless and
diffuse mesangial cell proliferation with
an increase in mesangial matrix
 Pathology
Polymorphonuclear leukocytes and
neutrophil are common in glomeruli
during the early stage of the disease.
Crescents and interstitial inflammation
may be seen in severe cases.
On electron microscopy, electron-dense
deposits, or “humps” are observed on the
epithelial side of the glomerular basement
membrances(GBMs)
In endocapillary proleferative GN,
“hump” appear outside of basement
 In endocapillary proliferative GN,
appear enlarged and bloodless
,mesangial proliferation and
5.Clinical manifestations

General manifestations
Antecedent infection
Typical manifestations
Severe manifestations
 Atypical manifestations
5.1 General manifestations
Many people with glomerulonephritis
have no symptoms
 When symptoms occur, they are often
flu-like, such as general fatigue, nausea,
vomiting, loss of appetite, fever, and
abdominal and joint pain.
These types of general symptoms can
continue for up to one month before
symptoms of kidney failure appear.
 5.2 Antecedent infection
90% patients have an
antecedent
streptococcal infection
Respiratory and skin
infections are chief
Typical manifestation is
6~12 days after
pharyngitis or 14~28
days after skin infection
 5.3 Typical manifestations
①Edema : 70% show
edema; unsunken;
face and eyelid upper
are generally involved
②Hemuturia:
50%~70% show gross
hematosis ,after
1~2wk, change into
microscopic
hematosis
 Typical manifestations
③Proteinuria: in general, <3g/d
④Hypertension:30%~80% show
hypertension, during preschool
age >120/80mmHg, school age
>130/90mmHg
Urine volume: decrease
Resolution should occur within 2
weeks , if not , consider other causes
 5.4 Severe manifestations
Severe cycle bloodshot

Hypertensive encephalopathy

Acute renal failure

①Severe cycle bloodshot
Cause: salt and water retention
cause blood volume increase
Alerting when AGN children show
tachypnea or moist crackles
Severe show dyspnea, gallop
rhythm, edema worsen, even die
②Hypertensive encephalopathy
Cause: vessel plasma
Hypertension suddenly ascend
>150~160/100~110mmHg
Symptoms: headache, vomiting,
diplopia, even convulsion, coma
After hypertension controlled,
these symptoms disappear
 ③Acute renal failure
Causes: mesangial cell
proliferation, blood capillary close
off, GFR↓
Symptoms: Oliguria or anuira,
electrolyte disturbances,
metabolic acidosis
 5.5 Atypical manifestations
AGN has no symptoms: only
microscopic hematouria, no other
clinical manifestations
AGN has symptoms out of kidney: has
streptococcal history, serum C3 level is
reduced, edema, hypertension is
notable, but urine routine is normal
AGN show nephritic syndrome: edema,
proteinuria is notable, but pathology
change is typical
 6. Laboratory evaluation
1. Urine routine ： proteinuria 1+~3+ ，
including RBC and cast
2. ASO↑
3. C3↓
4. ESR ↑
(erythrocyte sedimentation rate )
 Laboratory evaluation
5. A 24 hour urine collection allows
measurement of the excretion of
proteins and creatinine.
6. Creatinine clearance from the
bloodstream by the kidneys is
considered an index of the
glomerular filtration rate
 kidney biopsy
Kidney biopsy is essential to
establish a diagnosis of atypical
or prolonged AGN, determine the
cause, and create an effective
treatment plan and know its
prognosis
 7. Diagnosis
①For about 1~3wk before AGN has
streptococcal infection
②Clinical manifestations: edema,
hypertension, hematuria, proteinuria
③Urinalysis finding protein, RBC, cast
④Serum C3 level reduce and/or ASO↑
 8. Treatment
Goals of treatment

Principles of treatment
 Goals of treatment
Stop the ongoing inflammation and
lessen the degree of scarring that
ensues.
Decrease the damage to the glomeruli
Decrease the metabolic demands on
the kidneys
Improve kidney function.
 Principle of Management
• [No special therapy]
• 1. Bed Rest
Reduce activities according to the progress
of disease
2.Diet
Restrict fluid and daily salt intake
azotemia—restrict protein intake
Principle of Management
• 3.Antibiotic therapy—Penicillin7~10d
• 4.Symptomatic therapy
Edema---Diuretics
(furosemide, spironolactone)
Hypertention---Antihypertensive drugs
(nifepine)
Hypertensive Encephalopathy---sodium
nitroprusside
 Principle of Management
Kidney failure--- dialysis
Once kidney failure has occurred, waste
products must be removed from the bloodstream
for the kidneys through a process called dialysis.

A kidney transplant may also be an option.

 9. Prognosis

Recovery is >90%

 with <1% mortality in past

 chronic disease in 5-10%

 10. Prevention
Avoiding upper respiratory infections,
as well as other acute and chronic
infections, especially those of a
streptococcal origin.

Cultures of the infection site, usually

the throat, should be obtained and
antibiotic sensibility of the offending
organism determined.
 Prevention
Prompt medical assessment for
necessary antibiotic therapy should
be sought when infection is
suspected.
 The use of prophylactic
immunizations is recommended as
appropriate.