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