Acute Post

Streptococcal
Glomerulonephriti
s

Danica Alyssa C. Cruz, RMT

Acute Post Streptococcal
Glomerular Nephritis
– Acute poststreptococcal glomerulonephritis
(APSGN) results from an antecedent infection of
the skin (impetigo) or throat (pharyngitis)
caused by nephritogenic strains of group A beta-
hemolytic streptococci.  

– Acute poststreptococcal glomerulonephritis

occurs predominantly in males and often
completely heals, whereas patients with
rheumatic fever often experience relapsing
attacks.
 Pathophysiology

• Most forms of acute

in situ immune
glomerular poststreptococcal
trapping of
antigen-antibody glomerulonephritis (APSGN) are
circulating
complex
immune mediated by an immunologic
formation
complexes
process. Cellular and humoral
immunity is important in the
pathogenesis of this disease, and
humoral immunity particularly in
APSGN.
• Nonetheless, the exact mechanism
by which APSGN occurs remains to
be determined.

Acute Post Streptococcal

Glomerulonephritis
 Pathophysiology

1. in situ immune antigen-antibody complex formation

- A role for delayed-type hypersensitivity has been implicated
in the pathogenesis of this disease. Early in the course of
APSGN, resident endothelial and mesangial cells are
predominantly proliferated, and this is accompanied by
infiltration with polymorphonuclear leukocytes and
monocytes.
– Macrophages are effector cells that cause resident cellular
proliferation. The infiltration of macrophages in the
glomeruli is mediated by complement-induced chemotaxis
and, most likely, by an antigen-specific event related to
delayed-type hypersensitivity mediated by helper/inducer T
cells.
 Pathophysiology

2.  Glomerular trapping of circulating immune complexes

– the most widely proposed mechanism leading to the
development of APSGN. Nephritogenic streptococci produce
proteins with unique antigenic determinants. These antigenic
determinants have a particular affinity for sites within the
normal glomerulus.
– Following release into the circulation, the antigens bind to
these sites within the glomerulus. Once bound to the
glomerulus, they activate complement directly by interaction
with properdin.
– Properdin is a blood serum protein that participates in the
activation of complement in a pathway which does not involve
the presence of antibodies.
Clinical Symptoms and Signs

– The median age of presentation in childhood is age 6-8 years,

with the condition being extremely rare prior to age 2
years. In very young children, it is postulated that APSGN is
rare because of the low rate of streptococcal pharyngitis in
this age group and an immature immune response.
–  Males are 2 times more likely to have this condition
compared with females; the reason this difference in sex
prevalence is not known. However, the site of streptococcal
infection (pyoderma or pharyngitis) does not influence the
sex difference.
– The triad of edema, hematuria, and hypertension is classic
for APSGN.
 Clinical Symptoms and Signs

Both microscopic proteinuria the most frequent

and mild proteinuria may Edema and sometimes the
persist for several months
Proteinuria
only clinical finding
after the acute presentation.

The urine is usually reported in 50-90% of

described as being smoky, children who are
Hematuria Hypertension hospitalized with acute
cola colored, tea colored,
or rusty glomerulonephritis

Most serious early complication of this

Either bradycardia Circulatory Hypertensive disease. hypertension is usually severe
or tachycardia may congestion encephalopathy and is accompanied by signs of central
be observed. nervous system (CNS) dysfunction
 Laboratory test recommended
and its rationale

Complete Blood • Mild Anemia( Normocytic, Normochromic) in early phase

• Parallels the degree of extracellular fluid volume expansion
Count
• Usually Normal
WBC and Platelet • Occasional leukocytosis
count • Rarely, Mild Thrombocytopenia may be present

Lipid Profile , • Hypoproteinemia

• Hyperlipidemia
TPAG
 Laboratory test recommended
and its rationale
• Electrolyte Profile is usually normal
• Hyperkalemia and metabolic acidosis are only present in patient with
Serum Electrolytes significant renal impairment
• Total Calcium is low in patients who a have a nephrotic picture

• Elevation of BUN and creatinine is usually modest

BUN, Creatinine • Some patients may have severe azotemia at onset.

• Oliguria and Proteinuria is present.

• Urine is concentrated and acidic.
• Glucosuria occurs occasionally

Urinalysis •
•
Hematuria – most consistent urinary abnormality
Polymorphonuclear leukocytes, RE cells, Hyaline and/or Cellular cast are
present
• RBC casts – found in 60-85% of hospitalized children. Characteristic of
Glomerular lesion
 Laboratory test recommended
and its rationale

Streptococcal • An ASO titer of 250 U or higher is highly suggestive of recent

streptococcal infection
Antibody screening

Total • All complements are low during APSGN

• C3 has been found to be decreased in more than 90% patient during
Complement the first 2 weeks of the illness.

• Findings depend on the etiology of the acute glomerulonephritis, the

Renal Biopsy severity of the inflammatory process, and the stage of the disease at
the time of biopsy
Latest Technology for the
Diagnosis
Light Microscopy
- Glomerular tufts appears enlarged and swollen
-marked increased in proliferation of mesangial
and epithelial cells
-PMN leukocytes and monocytes are often
observed
-in severe cases, the glomeruli appears bloodless
-Granular deposits of IgG and C3 along the
capillary walls
-IgM, complement components, properdin and
fibrinogen are also often observed
Latest Technology for the
Diagnosis
Electron Microscopy
-electron densed deposits (humps) in the
sub epithelial space mostly in mesangial
notch near the GBM reflection over
mesangium
-during recovery, deposits rapidly
disappear, although fragments still maybe
found in mesangium
-in persistent disease, humps may not
disappear so rapidly
 Treatment

– The need for medicines in APSGN is usually limited in scope and

length.
• Antibiotics – Administer penicillin or erythromycin for 10 days to
ensure eradication of the streptococcus.
• Antihypertensive – not necessary after the child leaves the
hospital although mild hypertension may persist up to 6 weeks.
• Diuretic agents – rarely needed in the long term
THANK YOU! 