ACUTE POST-STREPTOCOCCAL
GLOMERULONEPHRITIS
Jeanne Marie H. Vales
Junior Intern
Emilio Aguinaldo College School of Medicine
APSGN
A classic example of the acute
nephritic syndrome
characterized by the sudden onset of gross
hematuria, edema, hypertension, and renal
insufficiency
NEPHROTIC SYNDROME
Proteinurea (>3.5g in 24hrs)
Urine looks frothy
++++ Protein
Hypoalbuminaemia
Albumin is lost in the urine
Due to gaps in Podocytes allowing
proteins to escape
Edema
Swelling around ankles & eyes
Due to loss of albumin
Intravascular oncotic pressure
Fluid moves out of vessels
Hyperlipidemia
Due to hypoalbuminaemia, the liver
compensates and increases production,
however this has the side effect of also
increasing the production of lipids,
hence causing hyperlipidaemia.
NEPHRITIC SYNDROME
Haematuria
Red cell casts distinguishing
feature, form in nephrons &
indicate glomerular damage
Podocytes develop large pores which
allow blood & protein through
Proteinurea
++ Protein (small amount)
Hypertension
Usually only mild
Low urine volume <300ml/day
Due to renal function been poor
ETIOLOGY
One of the most common glomerular
causes of gross hematuria in children
Caused by Group A -hemolytic
Streptococcus
Follows infection of the throat or skin
by certain nephritogenicstrains of
GABHS
Capsular M-protein defines whether the
bacterial strain is rheumatogenic or
nephritogenic
Nephritogenic strains are divided into
pharyngitis-associated serotypes (1, 3, 4,
12 and 49) and skin infection-associated
serotypes (2,49, 55, 57, and 60)
Most common in children ages 5-12 yr
and uncommon before the age of 3 yr
Twice more frequent in males than in
females
Usual sites of antecedent infection:
skin and the throat
Any location of streptococcal infection is
possible
PATHOPHYSIOLOGY
Inflammatory process that
takes place in the glomeruli
is triggered by antigenantibody reactivity that
results in local activation of
the complement system and
of the coagulation cascade
Immune complexes causing
glomerulonephritis may be
formed in circulation or in
situ in the glomerular
basement membrane
(GBM).
CLINICAL MANIFESTATIONS
Nephritic Syndrome (rarely nephrotic syndrome)
Occurs 1-2 weeks after an antecedent streptococcal
pharyngitis or 3-6 wk after a streptococcal pyoderma
Hematuria
Edema
Peripheral edema due to salt and water retention
Hypertension
Oliguria
Nonspecific symptoms such as malaise,
lethargy, abdominal pain, or flank pain are
common
DIAGNOSTIC
Urinalysis
Urinalysis demonstrates red blood cells, often in association
with red blood cell casts, proteinuria, and polymorphonuclear
leukocytes
Complete Blood Count
A mild normochromic anemia may be present from
hemodilution and low-grade hemolysis
ASO Titer Screening test
Serum C3 level
Significantly reduced in >90% of patients in the acute phase
Normalizes 6-8 weeks after onset
Serum CH50 - commonly depressed
Serum C4 - most often normal or only mildly depressed
Confirmation of the diagnosis requires clear
evidence of a prior streptococcal infection.
Positive throat culture
Rising antibody titer to streptococcal antigen(s)
confirms a recent streptococcal infection
Antistreptolysin O titer is commonly elevated
after a pharyngeal infection but rarely increases
after streptococcal skin infections.
Antideoxyribonuclease B level - best single
antibody titer to document cutaneous
streptococcal infection
COMPLICATIONS
Hypertension
Hypertension is seen in 60% of patients and is associated with
hypertensive encephalopathy in 10% of cases. Although the
neurologic sequelae are often reversible with appropriate
management, severe prolonged hypertension can lead to intracranial
bleeding.
Hypertensive encephalopathy must be considered in patients with
blurred vision, severe headaches, altered mental status, or new
seizures
Pulmonary Edema / Heart failure
Respiratory distress, orthopnea, and cough
Cerebral edema
Hyperkalemia, hyperphosphatemia, hypocalcemia, acidosis,
seizures, and uremia.
Acute renal failure can require treatment with dialysis.
TREATMENT SUPPORTIVE!
Management is directed at treating the
acute effects of renal insufficiency and
hypertension
Antibiotic therapy with penicillin x 10
days
Recommended to limit the spread of the
nephritogenic organisms
Does not affect the natural history of
APSGN.
Sodium restriction
Diuresis (usually with intravenous
furosemide)
Pharmacotherapy (hypertension)
Calcium channel antagonists
Vasodilators
Angiotensin-converting enzyme inhibitors
PROGNOSIS
Most patients with APSGN recover within 6
weeks with return of renal function
Majority show progressive healing and a good long-
term prognosis
The acute phase generally resolves within 6-8
weeks
Urinary protein excretion and hypertension
usually normalize by 4-6 weeks after onset
Persistent microscopic hematuria can persist for
1-2 years after the initial presentation
THANK YOU!
Reference: Nelson Textbook
of Pediatrics 20th Edition
