1. Acute Glomerular Nephritis
Mao Jianhua, Department of Nephrology, The Children’s Hospital of Zhejiang University School of Medicine

2. DEFINITION

3. 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.

4. Nephritogenic strains of β–hemolytic streptococci
ETIOLOGY
Nephritogenic strains of β–hemolytic streptococci

9. PATHOGENESIS
1. Immune complex glomerulonephritis caused by deposition of circulating 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.

15. Endocapillary proliferative nephritis
PATHOLOGY
Endocapillary proliferative nephritis

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

18. 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。

21. Immunofluorescence microscopy
Glomerular deposits of IgG and C3 in capillary and mesangium

25. 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.

28. Clinical Features

29. Classically: 1. Edema and oliguria
2. hematuria
3. hypertension

33. In some patients 1. Hypervolemia 2. Encephalopathy
3. Oilguric acute renal failure

34. LABORATORY FEATURE ■ Complement：C3, CH50 ■ Blood
■ Renal function examination
■ ESR
■ urinalysis
■ ASO, ADNase-B, Ahase, et al.

35. Differential diagnosis
Rapidly progressive glomerulonephritis
Chronic glomerulonephritis
Infection-associated glomerulonephritis not caused by streptococcus
Secondary glomerulopathies

36. TREATMENT

37. Treatment of acute PSGN is largely that of supportive care

38. 1. Stay in Bed
1. Stay in Bed

39. 2. DIET CONTROL
2. DIET CONTROL

40. 3. ANTIBIOTICS
3. ANTIBIOTICS

41. 4. Symptom control
diuretics and anti-hypertension therapy

42. 1. Congested circulation
2. Encephlopathy
3. Acute renal failure

43. PROGNOSIS

44. 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.

46. Acute Post-Streptococcal GN
Synonyms:
Acute proliferative glomerulonephritis, acute post-infectious GN.
Incidence:
Peak incidence in children (3-14). Sporatic, mostly winter and spring.
Etiology:
Glomerular trapping of circulating anti-streptococcal immune complexes. Group A, B-hemolytic streptococci, type 12.
Clinical:
Acute nephritic syndrome post-strept pharyngitis or pyoderma. Other infections.
Lab:
Nephritic urine with RBC casts. Evidence of streptococcal infection or serologic evidence of recent infection. Decreased serum complement.
Path:
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.
Clinical
Course:
Children - Excellent prognosis. Adults - Worse prognosis, some develop progressive disease.

47. Post-Streptococcal GN
CNS
Streptococcal
Infection
Latent Period
Acute Nephritis
+ Strep Assay
Hypertension
Edema
Proteinuria
Hematuria