SEMINAR

1. Acute post
streptococcal
glomerulonephritis
(APSGN)
R.Anusha
Pharm D VI Year
Roll No:170514882007.

2. Definition
• Acute inflammation of renal glomerular parenchyma due to
deposition of immune complexes characterized by sudden
onset of
Oliguria
Gross Hematuria (Sudden onset)
Hypertension
Edema

3. Incidence
• APSGN is most common in children aged 5-12 years
and uncommon before the age of 3 years.
• More common in boys than in girls.
• Male : Female ratio is 2:1.
• 2 to 4 % of pediatric admissions in India.
• 90% of renal disease of childhood.

4. Etiology
• PSGN follows infection of the throat or skin by certain
“nephritogenic” strains of group A β‐hemolytic
streptococci.
• Usually occurs
7 – 14 days after pharyngitis
2 weeks – 6 weeks after skin infection
• Epidemics of nephritis have been described in
association with throat (serotype M12) and skin
(serotype M49) infections.

6. Pathogenesis
Type III immunological reaction in which glomeruli are
damaged due to deposition of IgG antibody, antigen and
complement C3.

7. The two most widely proposed theories include
1)Glomerular trapping of circulating immune
complexes.
2)In situ immune antigen-antibody complex formation
resulting from antibodies reacting with either
streptococcal components deposited in the glomerulus or
with components of the glomerulus itself, which has
been termed “Molecular mimicry”.
• The resulting immune complex triggers complement
activation and inflammation.

8. Pathology
• The kidneys appear symmetrically enlarged.
• All glomeruli appear enlarged and relatively bloodless
and show diffuse mesangial cell proliferation with an
increase in mesangial matrix.
• Polymorphonuclear leukocytes are common in glomeruli
during the early stage of the disease.
• IF reveals lumpy-bumpy deposits of immunoglobulin
and complement on the glomerular basement
membrane(GBM) and in the mesangium.
• EM: electron-dense deposits, or “humps,” are observed
on the epithelial side of the GBM.

10. Clinical presentation

11. Diagnostic criteria of a APSGN
At least 2 of the following criteria must be present
• Positive throat or skin culture for streptococcus.
• Streptococcal products like antistreptolysin, antihyalironidase,
antiDNAse B, ASO titre are elevated (Anti – DNAse B is the single
most specific test for Stereptococcal infection)
• Hypocomplementemia: C3 decreased with in 2 weeks.

12. MANAGEMENT
• Treatment of APSGN is largely that of
Supportive care.
• Usually, patients undergo a spontaneous diuresis
within 7-10 days after the onset of their illness.
• Management is directed at treating the acute
effects of renal insufficiency and hypertension.

13. BED REST
 Bed rest is indicated as long as there are clinical
manifestations of active disease, such as edema,
hypertension or gross hematuria.
 The active phase generally resolves with in 2-3 days.
DIET
 The intake of sodium, potassium and fluids should be
restricted until blood levels of urea reduce and urine
output increases.

14. ANTIBIOTICS
 10-day course of systemic antibiotic therapy with
penicillin (once AGN occurred penicillin treatment has
no effect on course of disease----may be given if active
pharyngitis or pyoderma present).
WEIGHT
 Should lose about 0.5 % BW/ Day
 Fluid restriction is required in case of gain in weight.

15. DIURETICS
 Oral FUROSEMIDE( 1- 3 mg /kg) – for edema.
 IV FUROSEMIDE ( 2- 4 mg /kg) – pulmonary
edema.
 Some patients with substantial volume expansion
and marked pulmonary congestion do not respond to
diuretics. In those individuals, dialytic support is
appropriate.

16. HYPERTENSION
 Mild – restriction of salt and water
 Anti hypertensive agents –
AMLODIPINE
NIFEDIPINE
DIURETICS
 Hypertensive emergencies –
IV NITROPRUSSIDE or LABETALOL
ACUTE RENAL FAILURE
 Management of hypertension, hypervolemia,
electrolytes disorder and metabolic acidosis.

17. Indications for dialysis
• Persistant edema and hypertension refractory to the
therapy given.
• Persistant hyperkalemia.
• Severe metabolic acidosis unresponsive to medical
management.
• Neurological symptoms(altered mental status, seizures).
• BUN greater than 100-150 mg/dL.
• Calcium / phosphate imbalance , with hypocalcemic
tetany.

18. Outcome and prognosis
• Excellent prognosis(95%) in children with APSGN.
• Edema and BP ↓ - 1st week.
• Gross hematuria and significant proteinuria – Disappear
within 2 weeks.
• Hypertension subsides within 2-3 weeks.
• But urinalysis may be abnormal(persistant microscopic
hematuria) for several years.

19. Complications in severe cases
• Circulatory hypervolemia/Congestive heart failure
• Encephalopathy
• Acute renal failure

20. Reference:
• https://www.Medscape.com