Post-streptococcal glomerulonephritis (PSGN) is an immune-mediated kidney disease that usually develops 1-2 weeks after a streptococcal infection. It most commonly affects children ages 6-12 and is more prevalent in males. PSGN is caused by antibodies produced in response to a Group A streptococcal infection forming immune complexes in the kidneys. This can lead to edema, hematuria, proteinuria, and hypertension. Treatment focuses on supportive care, antibiotics, controlling blood pressure and preventing clotting to minimize complications. The prognosis is generally excellent in the short term, with most patients recovering fully within weeks, though a small percentage may develop chronic kidney disease long term.

1. Name :CHOW MIEN CHIN
Group :88
Post-streptococcal
glomerulonephritis (PSGN)

2. Epidemiology
Commonest cause of nephritic syndrome
Peak incidence age : age 6-12 y/o
Male : female ratio is 2:1
Immune mediated inflammation.
Most commonly-sporadic.

3. Etiology
Usually appear after infected by “nephritogenic”
Group A beta hemolytic streptococci (GAHS)-serotype
12,4,1.
GAHS typically can be found on skin and throat
Impetigo Strep. throat

4. Pathogenesis
Throat/skin infection by GAHS (serotype 12,4,1 )
Antibodies to streptococcus (anti-streptolysin O) are formed in the
circulation.
Antigen- antibody circulating immune complexes are deposited at
glomerular basement membrane

5. Acute nephritic syndrome develop
1-2
week
s
3-4
week
s
Streptococcus
pharyngitis
Streptococcus
pyoderma

6. Signs and symptoms
1) Edema (90%) : typically found on face, periorbital and
upper extremities.acites and anasarca mayb occur in
children.
2) Macroscopical hematuria (65%) : meat-colored
3) Proteinuria : usual ,normalize after 4 weeks
4) Hypertension (75%) : mild- moderate , subside after
diuresis.
5) Oligouria : in children <0.5mL/day/hr
(minimum urine output 0.5 -1 mL/day/hr)

7. Non specific symptoms :
Such as high blood pressure, tachycardia,anorexia, nausea
& vomit, general malaise, lethargy, low grade fever, pallor
due to edema/ anemia.

8. Complication in severe cases
1. Circulatory hypervolumia/congestive heart failure
2. Hypertensive encephalopathy
3. Acute renal failure
4. Pulmonary edema

9. Lab. investigation
1. Urinalysis
2. Bacteriological and serological test
3. Renal function test
4. Full blood count
5. Serum complement level

10. Urinalysis
Macroscopic hematouria : rusty / tea- colour.
Microscopic hematouria:leucocyte, RBC casts
Pyuria :fibrin degrade products.
Evidences of streptococcus infection
• Skin and throat culture.
• high (anti-streptolysin)O and (anti-deoxyribonuclease)B titer
Renal f(n) test
• Increased creatinine, BUN level.
• Decrease GFR unlikely to be found in children.
• Hyperkalemia, hypocalcaemia, metabolic acidosis and
hyponatremia seen only in severe patients.

11. FBC
• Mild normochromic anemia ,leucocytosis mayb present.
Activation of complements
• Serum C3 lvl decrease (90%) , return to normal within
6weeks.
• Serum C4 lvl are typically normal.
*complement-group of protein work with immune system and
move freely in bloodstream, complement level decrease
during inflammation.*

12. Electron microscope
Immune deposits on the epithelial side of glomerular
basement membrane form “Humps” .

13. Immunofluoroscence microscopy
Granular (lumpy, bumpy) deposition of C3 and IgG alone
the capillaries loops and the mesangium.

14. Differential diagnosis
Ig A Nephropathy
Hematouria
Crescentic glonerulonephritis
Diffuse proliferative glomerulonephritis
Chronic nephritis

15. Treatment
Treatment of PSGN is mainly on supportive care, restriction
of fluid and sodium.
Usually patient undergo spontaneous diuresis within 7-10
days aft onset of illness.
10 days systemic AB therapy with penicillin V to limit the
spread of nephritogenic organisms.
Management is direct to treat the acute effect of renal
insufficiency and HPT.

16. Anti-hypertensive :

17. **Anti- aggregant & anti-coagulant are given to prevent micro-
thrombosis.**
Anti- aggregant :
(eg: aspirin, dipyridamole, clopidegol)
Anti –coagulant:
(eg: heparin) subcutaneously or I.V, 2-4times/day
 Extra- corporal method:
(eg: plasmapheresis are given to remove immune complexeswith
combination of strong medication.)
 Pulse therapy:

18. Complication
Nephrosclerosis.

19. Prognosis
Short term outcome : excellent, mortality <0.5%
Long term outcome : 2% children deve. Chronic kidney
disease.