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Acute Glomerular Nephritis

Acute Glomerular Nephritis. Mao Jianhua, Department of Nephrology, The Children Hospital of Zhejiang University, maojh88@gmail.com. DEFINITION.

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Acute Glomerular Nephritis

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  1. Acute Glomerular Nephritis Mao Jianhua, Department of Nephrology, The Children Hospital of Zhejiang University, maojh88@gmail.com

  2. DEFINITION • APSGN is a immune-mediated inflammation disease with the mechanism for proliferative glomerulonephritis affecting almost all nephrons in both kidney in patients.

  3. EPIDEMIOLOGY APSGN is a disease that affects primarily children, with the peak incidence being between ages of 2 and 12 years, Males are more likely than females to have overt nephritis. Crowded conditions, poor hygiene, malnutrition, and intestinal parasites may results in epidemic outbreaks. APSGN is on the decline in developed countries.

  4. ETIOLOGY Nephritogenic strains of group Aβ–hemolytic streptococci: type Ⅻ Other than streptococci, staphylococci, gram-negative rods, and intracellular bacteria also associated with a post-infectious glomerulonephritis recently.

  5. Pharyngitis

  6. scarlet fever

  7. Impetigo

  8. 毛建华

  9. PATHOGENESIS Despite the early recognition of an association between streptococcal infection and an acute glomerulonephritis, the pathogenic mechanism of disease remains incompletely understood.

  10. 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 self-antigen or neo-antigen. 3. Immune complexes are formed in situ in the mesangium in response to a planted antigen.

  11. PATHOLOGY Endocapillary proliferative nephritis

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

  13. Immunofluorescence microscopy Granular deposits of IgG and C3 in capillary loops and mesangium

  14. Electron microscopy 1.The proliferation of cells is seen to involve primarily endothelial cells and the mesangium. 2.Electron-dense humplike dense deposits on the epithelial side of the basement membrane.

  15. Clinical Features

  16. Latent period: Averages 10 days after a pharyngitis (range 7 to 21 days) May be longer after a skin infection (range 14 to 21 days) Short latent period of less than 7 days presented in patient with?

  17. Classically, the syndrome of APSGN presents abruptly with hematuria, edema, azotemia and hypertension. The syndrome can present with an entire spectrum of severity from asymptomatic to oliguric acute renal failure.

  18. Classically: 1. oliguriaand edema: based on renal fluid & sodium retention. 2. microscopic/gross hematuria 3. hypertension: occurs in more than 75% patients, usually mild to moderate.

  19. In some patients 1. Hypervolemia & congestive heart failure 2. Encephalopathy: confusion, headache, somnolence 3. Oliguric acute renal failure

  20. Edema & hypertension typically resolve in 1 to 2 weeks after diuresis, though hematuria and proteinuria may persist for several months, but they usually resolve within 1 year.

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

  22. Dennen P, Douglas I, Anderson R,: Acute Kidney Injury in the Intensive Care Unit: An update and primer for the Intensivist. Critical Care Medicine 2010; 38:261-275.

  23. Differential diagnosis • Rapidly progressive glomerulonephritis • C3 related glomerular nephropathy • Chronic glomerulonephritis • Infection-associated glomerulonephritis not caused by streptococcus • Secondary glomerulopathies: IgAN

  24. A．确诊病例：需要实验室的确诊依据，或实验室提示依据+临床证据；A．确诊病例：需要实验室的确诊依据，或实验室提示依据+临床证据； B．疑似病例：仅需要临床证据； C．可能病例：仅需要实验室提示依据； 实验室确诊依据是指肾活检证实为APSGN（内皮细胞增殖，伴系膜区及沿肾小球毛细血管袢的颗粒状沉积[8]）； 实验室提示依据包括同时符合以下三条：①镜检血尿：红细胞>10个/高倍视野；②近期链球菌感染的依据（链球菌培养阳性，或ASO升高，或抗DNase-B阳性）；③补体C3降低。 临床证据包括以下四条中至少两条：①面部水肿；②中等程度以上的血尿；③高血压；④外周肢体水肿。

  25. TREATMENT

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

  27. 1. Bed Rest

  28. 2. DIET CONTROL 2. DIET CONTROL

  29. 3. ANTIBIOTICS 3. ANTIBIOTICS

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

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

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