Acute Glomerular Nephritis

Mao Jianhua, Department of Nephrology, The Children’s Hospital

of Zhejiang University School of Medicine

DEFINITION

EPIDEMIOLOGY

APSGN is a disease that affects primarily children, with the peak incidence being between ages of 2 and 6 years, Males are more likely than females to have overt nephritis.

ETIOLOGY

Nephritogenic strains of β–

hemolytic streptococci

PATHOGENESIS 1. Immune complex glomerulonephritis caused by deposition of cir

culating antigen-antibody complexes.

2. Autoimmune glomerulonephritis caused by deposited IgA being directed against a mesangial antigen or neo-antigen.

3. Immune complexes are formed in situ in the mesangium in response to a planted antigen.

PATHOLOGY

Endocapillary proliferative nephritis

Light microscopy

the glomeruli are found to be swollen and filled with cells obscuring much of the delicate network of the normal glomerular tugt.

正常肾小球，用 PAS 染色以突出基底膜。肾小球血管袢薄而清晰。

Immunofluorescence microscopy

Glomerular deposits of IgG and C3 in c

apillary and mesangium

Electron microscopy

1.The proliferation of cells is seen to involve

primarily endothelial cells and the

mesangium.

2.Electron-dense humps on the epithelial

side of the basement membrane.

Clinical Features

Classically: 1. Edema and oliguria

2. hematuria

3. hypertension

In some patients

1. Hypervolemia

2. Encephalopathy

3. Oilguric acute renal failure

LABORATORY FEATURE

■ Complement ： C3, CH50

■ Blood

■ Renal function examination

■ ESR

■ urinalysis

■ ASO, ADNase-B, Ahase, et al.

Differential diagnosis Rapidly progressive glomerulonephritis

Chronic glomerulonephritis

Infection-associated glomerulonephritis not caused by streptococcus

Secondary glomerulopathies

TREATMENT

Treatment of acute PSGN is largely that of supportive care

1. Stay in Bed1. Stay in Bed

2. DIET CONTROL2. DIET CONTROL

3. ANTIBIOTICS3. ANTIBIOTICS

4. Symptom control

diuretics and anti-hypertension therapy

1. Congested circulation

2. Encephlopathy

3. Acute renal failure

PROGNOSIS

Most children (up to 95%) fully recover from

APSGN in a matter of weeks or months. In those who

do not recover fully, chronic or progressive problems

of kidney function may occur. Kidney failure may

result in some patients.

Acute Post-Streptococcal GNAcute Post-Streptococcal GN

Synonyms:

Incidence:

Etiology:

Clinical:

Lab:

Path:

ClinicalCourse:

Acute proliferative glomerulonephritis, acute post-infectious GN.

Glomerular trapping of circulating anti-streptococcal immune complexes. Group A, B-hemolytic streptococci, type 12.

Acute nephritic syndrome post-strept pharyngitis or pyoderma. Other infections.

Nephritic urine with RBC casts. Evidence of streptococcal infection or serologic evidence of recent infection. Decreased serum complement.

Children - Excellent prognosis. Adults - Worse prognosis, some develop progressive disease.

Enlarged, hypercellular glomeruli with endothelial and mesangial cell proliferation. Acute inflammation. IgG and C3 in very coarsely granular pattern along GBMs. Discrete, subepithelial “hump-like” deposits.

Peak incidence in children (3-14). Sporatic, mostly winter and spring.

Post-Streptococcal GNPost-Streptococcal GN

CNS

+ Strep Assay

Hypertension

Proteinuria

Hematuria

StreptococcalInfection

Latent Period

Acute Nephritis

Edema