Poststreptococcal acute glomerulonephritis (AGN) is a common condition in childhood caused by a Streptococcus pyogenes infection. It involves an immune response that leads to inflammation of the glomeruli in the kidneys. Symptoms include edema, gross hematuria, hypertension, and acute renal insufficiency. Treatment focuses on controlling blood pressure, restricting fluid and salt intake, and administering antibiotics. While early AGN is often temporary and reversible, chronic glomerulonephritis can lead to permanent kidney damage if not properly managed.

1. Dr. Sunil Natha Mhaske
Dean And Professor (Paediatrics)
Dr. Vithalrao Vikhe Patil Foundation’s Medical College And Hospital, Ahmednagar,
Maharashtra, India
in children

2. • Glomerulonephritis (GN) is inflammation of the glomeruli of Kidney.
• GN can be both acute, chronic and Rapidly progressive.
• This condition used to be known as Bright’s disease.
The symptoms and signs of Bright's disease were first described in
1827 by the English physician Richard Bright, after whom the disease
was named.

4.  Poststreptococcal acute Glomerulonephritis or Acute glomerulonephritis (AGN) is a
common condition in childhood.
 Immune mediated inflammation of glomerules in childhood.
 Typical age is 2-12 years.
 Patients usually have streptococcal pharyngitis or impetigo 5-21 days before AGN
manifestation.
 It is caused by Streptococcus pyogenes infection.
 Incidence is 6–20:1,00,000 in western countries
 Risk factors :
 gender (more frequent in boys)
 Lower hygienic standard
 malnutrition.
 Genetic predisposition
 Nephritogenic beta-hemolytic streptococcus, group A, type M 12 and 49 -originator.

5. Antigens produced by Streptococcus pyogenes - NSAP-
streptokinase (nephritogen strains associated protein), M-
protein and endostreptosin.
These antigenes are binded by specific antibodies.
So created immunocomplexes are taken up in capillaries of
glomerules as deposites.
It is mediated by activation of complement too.
Finally, it leads to proligerative glomerulonephritis with
decreased glomelural filtration, higher natrium resorption in
tubules (→ edema), increased renin secretion (→
hypertension).
Pathophysiology

7. • Edema
- 75% of patients
- Acute onset.
- Mild to modest severity.
- Pitting edema.
- Starts in the eyelids and face then the lower and upper limbs then generalized (Hydrocele, ascites.
Pericardial and pleural effusion.)
- It may be migratory: appear in eyelid in the morning, disappear in the afternoon and reappear
around the ankle in the ambulant patients by the end of the day.
 Gross hematuria (65%) - tea colored or cola colored urine;
 Hypertension (50%)
 Acute renal insufficiency
 Oliguria-Urine output is less than 400 ml/day - 0 .5ml/hour/day
 Hypertension.
 General- Fever, Pallor, headache, malaise, anorexia, nausea and vomiting.
Clinical features-

8. Illnesses which triggers acute GN-
 Strep throat
 Systemic lupus erythematosus (lupus)
 Goodpasture syndrome- a rare autoimmune disease in which antibodies attacks kidneys
and lungs.
 Amyloidosis -when abnormal proteins harms organs and tissues.
 Granulomatosis with polyangiitis (Wegener’s granulomatosis)- inflammation of the blood
vessels.
 Polyarteritis nodosa-cells attack arteries.
 Heavy use of nonsteroidal anti-inflammatory drugs-ibuprofen and naproxen.

9.  develop over several years with no or very few symptoms.
 This can cause irreversible damage to your kidneys and ultimately lead to complete kidney failure.
 Chronic GN doesn’t always have a cause.
 Hereditary nephritis
 Other possible causes include:
 certain immune diseases
 a history of cancer
 exposure to some hydrocarbon solvents
 acute form of GN may make you more likely to develop chronic GN later on.
 Clinical features-
 blood or excess protein in urine.
 high blood pressure.
 swelling in ankles and face.
 frequent night time urination.
 abdominal pain.
 frequent nosebleeds.
Chronic GN

10. 1. Urine assay-
 Hematuria
 Urine color- “coke,” “tea,” or “smoky” colored.
 Urine color in agn is uniform throughout the stream.
 Mild to moderate proteinuria-1 + to 2+ protein.
 Concentrated urine
 Presence of casts
 Urine culture.
 Creatinine clearance
 Urine specific gravity
 Urine osmolality
Diagnosis

11. 2. Blood examination-
- Elevated creatinine.
- ASO antibodies
- Reduced serum C3 level
- Elevated serum IGM and IGG
- Anemia –hemodilution
- Abnormal albumin levels
- E.S.R. increased.
- Blood of urea elevated
3. Immunology -
 Antiglomerular basement membrane antibodies
 Antineutrophil cytoplasmic antibodies
 Antinuclear antibodies
 Complement levels

12.  CT scan
 Kidney ultrasound
 Chest X-ray
 Intravenous pyelogram
 Renal biopsy is not indicated.

13. Hematuria in Children
• Hematuria means that red blood cells are in the urine.
• Urine does not normally contain red blood cells because the filters in the kidney prevent
blood from entering the urine.
• In hematuria, the filters or other parts of the urinary tract allow blood to leak into the
urine.
• Gross hematuria -urine appears red or the color of tea or cola.
• Microscopic hematuria -urine microscopic examination findings of red blood cells
(RBCs) of more than 5/µL in a fresh uncentrifuged midstream urine specimen or more
than 3 RBCs/high-power field (HPF) in the centrifuged sediment from 10 mL of freshly
voided midstream urine.

14. Causes of hematuria -
A. Glomerular diseases-1) Recurrent gross hematuria (IgA nephropathy, benign familial
hematuria and Alport’s syndrome); 2) acute poststreptococcal glomerulonephritis; 3)
membranoproliferative glomerulonephritis; 4) systemic lupus erythematosus; 5) membranous
nephropathy; 6) rapidly progressive glomerulonephritis, Henoch-Schonlein purpura and
Goodpasture’s disease.
B. Interstitial and tubular-1) acute pyelonephritis; 2) acute interstitial nephritis; 3)
tuberculosis.
C. Hematologic causes-Sickle cell disease, coagulopathies, von Willebrand’s disease, renal
vein thrombosis and thrombocytopenia.
D. Urinary tract-1) bacterial or viral infection, 2) nephrolithiasis; 3) hypercalciuria.
E. Structural anomalies-Congenital anomalies and polycystic kidney disease.
F. Trauma, tumors and exercise.
G. Medications- Aminoglycosides, amitryptiline, anticonvulsants, aspirin, chlorpromazine,
coumadin, cyclophosphamide, diuretics, penicillin and thorazine.

17.  Hospitalization
 Monitor blood pressure and urine output
 Checking of weight daily
 Blood for urea, creatinine, sodium and potassium.
 Anti-hypertensive drugs
 Restrict fluid intake till urine output improves.
 Intake of salt needs to be restricted
 Avoid intake of substances containing high potassium like fruits and tender coconut.
 A course of appropriate antibiotic is needed to eradicate infection.
Management-

18.  Acute kidney failure
 Chronic kidney disease
 Electrolyte imbalances, such as high levels of sodium or potassium
 Chronic urinary tract infections
 Congestive heart failure due to retained fluid or fluid overload
 Pulmonary edema due to retained fluid or fluid overload
 High blood pressure
 Malignant hypertension, which is rapidly increasing high blood
pressure
 Increased risk of infections
Complications-

19.  Early, acute GN can be temporary and reversible.
 Chronic GN may be slowed with early treatment.
 Complete remission is in 95% of patients.
 only 5% of all patients can progress to end stage renal disease.
Prognosis-