2. Objectives
• To know the causes of hematuria
•The causes of proteinuria
•To differentiate between nephrotic and
nephritic syndromes
3. Acute poststreptococcal glomerulonephritis
• It is characterized by sudden onset of gross
hematuria, edema, hypertension and renal
insufficiency.
• It is the second most common cause of gross
hematuria after IgA nephropathy.
4. Etiology:
• It follows infection of the throat (cold weather) or
skin (warm weather) by certain nephritogenic
strain of group A beta hemolytic streptococci.
Pathology:
• evidence suggests that immune complexes,
preformed by the combination of specific
antibodies against streptococcal antigens, localize
on the glomerular capillary wall and activate the
complement system.
5. Immunofluorescence microscopy :
• reveals a lumpy-bumpy deposits of
immunoglobulin and complements on the GBM.
Electron microscopy:
• there is electron dense deposits or humps on the
epithelial side of GBM .
On light microscopy:
• All glomeruli appear enlarged with diffuse
mesangial cell proliferation with increase in the
mesangial matrix
6. Clinical manifestations:
• It is most common in children 5-12 years old and
uncommon before the age of 3 years.
• Male-to-female ratio is 2:1
• The typical nephritis syndrome occurs 1-2 weeks
after a strep. Pharyngitis or 3 weeks after strep.
Pyoderma.
• Presentations may vary from asymptomatic
microscopic hematuria to acute renal failure.
7. • There is a various degree of edema in 85% of cases
(due to salt and water retention) starts as
periorbital then may become generalized.
• Gross hematuria occurs in 30-50% of patients. The
urine is usually described as being smoky, cola
colored, tea colored, or rusty.
• Oliguria may be noted.
8. • Hypertension is the third cardinal feature of
PSAGN and is reported in 50-90% of children
who are hospitalized with AGN.
• Hypertension is multifactorial and may be
related to ECF volume expansion.
• Hypertensive encephalopathy has been
reported in approximately 5% of hospitalized
children and is the most serious early
complication of this disease.
9. • Dyspnea, orthopnea, and cough may be present.
• Pulmonary rales are often audible.
• Also there may be fever, malaise, lethargy and
abdominal pain
• The acute phase resolves within 6-8 weeks.
• The urinary protein excretion and hypertension
normalize by 4-6 weeks after the onset but
microscopic hematuria may persist 1-2 years.
10. Diagnosis:
1. Urinalysis show:
• RBC and RBC cast, hyaline cast.
• proteinuria 3+ by dipstick, corresponding
to fewer than 2 g/m2/d.
11. 2. Evidence for streptococcal infection:
• Cultures from either the pharynx or skin may be
positive.
• Antibodies to a variety of streptococcal antigens
(eg, Antistrepolysin O, Antihyalurinidase Ab, anti-
DNase B).
• A mild anemia (normocytic, normochromic) is
common due to hemodilution and low grade
hemolysis.
12. • Serum complement C3 level is reduced in the
acute phase and returns to normal 6-8 weeks
after the onset.
• Mild elevation of blood urea and creatinine.
Electrolytes are normal except in patients with
RF.
• Renal biopsy is indicated only in:
a-Acute RF b-Nephrotic syndrome c-Absent
evidence for strep. Infection
d-Normal complement C3 level or if remain low
2 mo after the onset
13. Differential diagnosis:
Other causes of hematuria:
A-Glomerular hematuria:
1. IgA nephropathy (Burger
disease).
2. Alport syndrome
(hereditary nephritis)
3. Membranous
nephropathy
4. Membranoproliferative
GN
5. Focal segmental GN
6. Henoch-Schonlein
purpura
7. SLE nephritis
8. Hemolytic uremic
syndrome
9. Sickle cell
glomerulopathy
15. Complications:
1. Hypertensive encephalopathy manifested
by headache, vomiting, depressed
sensorium, confusion, visual disturbances,
aphasia, memory loss, coma, and
convulsions.
2. Acute renal dysfunction with increase urea,
creatinine, hyperphosphatemia,
hypocalcaemia and acidosis.
3. Heart failure and pulmonary congestion.
16. Prognosis:
• Complete recovery occurs in more than 95%
of cases
• Recurrences are extremely rare.
Prevention:
• Early systemic antibiotic therapy for strep.
Infection does not eliminate the risk of GN.
17. Treatment:
• 10 days course of penicillin is recommended
to limit the spread of nephritogenic
organisms. Dose <12 years: 25-50 mg/kg/d
PO divided tid/qid
• Hospitalization is indicated if the child has
significant hypertension or a combination of
oliguria, generalized edema, and elevation of
serum creatinine or potassium.
18. • Mild-to-moderate hypertension is treated
most effectively with bed rest, fluid
restriction, and
• small dose of antihypertensive medications
such as furosemide (1-3 mg/kg/d PO,
administered 1-2 times daily)
• For patients resistant to treatment, either
hydralazine or nifedipine is indicated.
19. • Angiotensin-converting enzyme inhibitors
(ACEI) are effective, although they have the
potential to produce hyperkalemia and
usually are not first-line drugs in AGN.
• Diet: A low-sodium, low-protein diet should
be prescribed during the acute phase, when
edema and hypertension present.
