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ACUTE
GLOMERULONEPHRITIS
(AGN)
DHARSHINI JEYAMOHAN
GLOMERULUS
Glomerular disease includes
glomerulonephritis, i.e. inflammation of
the glomeruli and glomerulopathies when
there is no evidence of inflammation.
Glomerulonephritis is a subset of
glomerulopathies
Acute glomerulonephritis (AGN) is an
abrupt onset of one or more features of an
Acute Nephritic Syndrome :
• Oedema e.g. facial puffiness
• Microscopic / macroscopic haematuria
• Decreased urine output (oliguria)
• Hyprtension
• Azotemia
Acute Glomerulonephritis
Presenting features of AGN
Acute nephritic syndrome (most common)
Nephrotic syndrome
Rapidly progressive glomerulonepritis
Hypertensive encephalopathy
Pulmonary oedema
Subclinical (detected on routine
examination)
Causes of Acute Nephritis
Post streptococcal AGN
Post-infectious acute glomerulonephritis (other
than Grp A B-Haemolytic Stretococci)
Subacute bacterial endocarditis
Henoch- Schoelein Purpura
IgA nephropathy
Hereditary nephritis
SLE
Systemic vasculitis
Lupus
In children, the commonest cause of acute
nephritic syndrome is post-infectious
AGN, mainly due to post-streptococcal
infection of the pharynx or skin.
Post streptococcal AGN is commonest at
6-10 years age.
ACUTE
POST-STREPTOCOCCAL
GLOMERULONEPHRITIS
Definition
AGN that follows an infection with a
nephritogenic strain of group A beta
hemolytic streptococci.
The classic example of the acute nephritic
syndrome.
Nelson Textbook of Pediatrics, 7th
Edition
Streptococcal infection of the throat
( strep throat) or skin ( impetigo)
EpidEmiology
 121 of the 124 patients had poststreptococcal
nephritis.
Department of Pediatrics, HUSM, July 1987- June 1988
 Globally - incidence has decreased in the past
three decades.
 Most commonly – sporadic.
 Despite that, epidemics and clusters of cases - in
some poor or rural communities
© 2008 American Society of Nephrology
 Peak incidence - age 5-12 y/o, uncommon <3y/o.
 Male : female ratio is 2 : 1.
(Nelson Textbook of Pediatrics, 7th
Edition)
Etiology and
pathogEnEsis
 The child gets throat or skin infection by nephritogenic
strain of group A beta hemolytic streptococci - serotype
12 , 4 and 1
 Antibodies to streptoccocus (eg antistreptolysin O) are
formed in the circulation
 Antigen-antibody circulating immune complexes are
subsequently deposited along the glomerular basement
membrane (GBM).
Streptococcal infection
immune complex formation + deposited in GBM
complement system activated
immune injuries
cellular proliferation GBM fracture
capillary lumen narrowed hematuria
glomerular blood flow decreased proteinuria
oliguria GFR↓ distal sodium reabsorption
retention of water & sodium
blood volume ↑
edema
hypertension
Low serum
complement
typical manifEstation
Develop acute nephritic syndrome 1–2 wk after an antecedent
streptococcal pharyngitis or 3–6 wk after a streptococcal
pyoderma.
1.Edema
75% of the patients
Face, periorbital area  lower extremities  generalized
(ascites, pleural effusions)
2. Proteinuria – usually normalize after 4 weeks
3. Oliguria
school child < 400ml/day
preschool child < 300ml/day
infant & toddler < 200ml/day
typical manifEstation
3. Gross hematuria (65% of patients)
Smoky, tea-colored, cola-colored, or fresh bloody urine
Microscopical hematuria (almost all patients)
The urine appears normal, but >3 RBCs/HP are found in
centrifuged urine sediment examined microscopically.
4. Hypertension (50%) – mild to moderate, typically
subsides promptly after diuresis
5. Nonspecific symptoms:
Such as anorexia, vomiting, general malaise, lethargy,
abdominal or flank pain, low-grade fever and weight
gain.
Clinical course
Spontaneous improvement typically begins within 1 wk
with resolution of edema in 5-10 days and hypertension
in 2-3 wk, but urinalysis may be abnormal (persistent
microscopic hematuria) for a year.
invEstigations
Urinalysis and culture
• Haematuria – present in all patients.
• Proteinuria (trace to 2+, but may be in the
nephrotic range; usually associated with more
severe disease.)
• Red blood cell casts (pathognomonic of acute
glomerulonephritis).
• Other cellular casts.
• Pyuria may also be present.
invEstigations
 Bacteriological and serological evidence of antecedent
streptococcal infection:
• Raised ASOT ( > 200 IU/ml ).
• Increased anti-DNAse B (if available) – a
better serological marker of preceding
streptococcal skin infection.
• Throat swab or skin swab.
 Renal function test
• The BUN concentration is elevated in 75% of patients, and
serum creatinine level is increased in one half of the patients, but
profound decrease in GFR is uncommon in children.
• Hyperkalemia, hypocalcaemia, hyponatremia, and metabolic
acidosis are seen only in severe patients.
InvestIgatIons
 Full blood count
• A mild normochromic anemia may be present from
hemodilution and low-grade hemolysis.
• Leucocytosis may be present.
 Complement levels
• C3 level – low at onset of symptoms, normalizes by 6wks
• C4 is usually within normal limits in post-streptococcal
AGN.
 Ultrasound of the kidneys
• Not necessary if patient has clear cut acute nephritic
syndrome.
IndIcatIons for
renal
BIopsy
 Severe acute renal failure requiring dialysis.
 Features suggesting non post-infectious AGN as the
cause of acute nephritis.
 Delayed resolution
• Oliguria > 2 weeks
• Azotaemia > 3 weeks
• Gross haematuria > 3 weeks
• Persistent proteinuria > 6 months
lIght mIcroscope
not specIfIc for post streptococcal nephrItIs
•Glomeruli appear enlarged and hypercellular.
•Diffuse mesangial cell proliferation with an increase in mesangial
matrix.
•Polymorphonuclear leukocytes are common in glomeruli during
the early stage of the disease.
dIagnosIs
Acute onset
Symptoms: edema, oliguria, dark urine,
hypertension
Urinalysis: RBCs, protein, casts
Evidences of streptococcal infection:
– Prodromes
– Elavated serum titers of Abs to
streptozymes(ASO)
Serum C3 - Reduced
dIfferentIal
dIagnosIs
dIfferentIal dIagnosIs
management
Strict monitoring - fluid intake, urine output,
daily weight, BP (Nephrotic chart)
Penicillin V for 10 days to eliminate β -
haemolytic streptococcal infection (give
erythromycin if penicillin is contraindicated)
Fluid restriction to control oedema and
circulatory overload during oliguric phase
until child diureses and blood pressure is
controlled
management
• Day 1 : up to 400 mls/m²/day. Do not administer
intravenous or oral fluids if child has pulmonary
oedema.
• Day 2 : till patient diureses – 400 mls/m²/day (as long
as patient remains in circulatory overload)
• When child is in diuresis – free fluid is allowed
Diuretic (e.g. Frusemide) should be given in
children with pulmonary oedema. It is also
usually needed for treatment of hypertension.
Diet – no added salt to diet. Protein restriction is
unnecessary
complIcatIons
Look out for complications of post-
streptococcal AGN:
• Hypertensive encephalopathy usually
presenting with seizures
• Pulmonary oedema (acute left ventricular
failure)
• Acute renal failure
management for
complIcatIons
Significant asymptomatic
hypertension
symptomatic, severe hypertension or hypertensive emergency /
encephalopathy
Prehypertension is defined as a blood pressure
in at least the 90th percentile, but less than the
95th percentile, for age, sex, and height, or a
measurement of 120/80 mm Hg or greater.
Hypertension is defined as blood pressure in
the 95th percentile or greater.
Acute pulmonary edema
MANAGEMENT for
coMplicATioNs
MANAGEMENT for
coMplicATioNs
Acute Renal Failure
follow-up
 For at least 1 year.
Monitor BP at every visit
Do urinalysis and renal function to
evaluate recovery.
Repeat C3 levels 6 weeks later if not
already normalised by the time of
discharge.
ouTcoME
 Short term outcome: Excellent, mortality
<0.5%.
 Long term outcome: 1.8% of children
develop chronic kidney disease following
post streptococcal AGN.
 These children should be referred to the
paediatric nephrologists for further
evaluation and management.
sourcEs
Paediatric Protocols 3rd
Edition
Nelson Textbook of Pediatrics, 7th
Edition
Renal Unit , Royal Hospital for Sick
Children , Yorkhill Division
© 2008 American Society of Nephrology
THANK
You

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AGN

  • 3. Glomerular disease includes glomerulonephritis, i.e. inflammation of the glomeruli and glomerulopathies when there is no evidence of inflammation. Glomerulonephritis is a subset of glomerulopathies
  • 4.
  • 5. Acute glomerulonephritis (AGN) is an abrupt onset of one or more features of an Acute Nephritic Syndrome : • Oedema e.g. facial puffiness • Microscopic / macroscopic haematuria • Decreased urine output (oliguria) • Hyprtension • Azotemia Acute Glomerulonephritis
  • 6. Presenting features of AGN Acute nephritic syndrome (most common) Nephrotic syndrome Rapidly progressive glomerulonepritis Hypertensive encephalopathy Pulmonary oedema Subclinical (detected on routine examination)
  • 7. Causes of Acute Nephritis Post streptococcal AGN Post-infectious acute glomerulonephritis (other than Grp A B-Haemolytic Stretococci) Subacute bacterial endocarditis Henoch- Schoelein Purpura IgA nephropathy Hereditary nephritis SLE Systemic vasculitis
  • 9. In children, the commonest cause of acute nephritic syndrome is post-infectious AGN, mainly due to post-streptococcal infection of the pharynx or skin. Post streptococcal AGN is commonest at 6-10 years age.
  • 11. Definition AGN that follows an infection with a nephritogenic strain of group A beta hemolytic streptococci. The classic example of the acute nephritic syndrome. Nelson Textbook of Pediatrics, 7th Edition
  • 12. Streptococcal infection of the throat ( strep throat) or skin ( impetigo)
  • 13. EpidEmiology  121 of the 124 patients had poststreptococcal nephritis. Department of Pediatrics, HUSM, July 1987- June 1988  Globally - incidence has decreased in the past three decades.  Most commonly – sporadic.  Despite that, epidemics and clusters of cases - in some poor or rural communities © 2008 American Society of Nephrology  Peak incidence - age 5-12 y/o, uncommon <3y/o.  Male : female ratio is 2 : 1. (Nelson Textbook of Pediatrics, 7th Edition)
  • 14. Etiology and pathogEnEsis  The child gets throat or skin infection by nephritogenic strain of group A beta hemolytic streptococci - serotype 12 , 4 and 1  Antibodies to streptoccocus (eg antistreptolysin O) are formed in the circulation  Antigen-antibody circulating immune complexes are subsequently deposited along the glomerular basement membrane (GBM).
  • 15. Streptococcal infection immune complex formation + deposited in GBM complement system activated immune injuries cellular proliferation GBM fracture capillary lumen narrowed hematuria glomerular blood flow decreased proteinuria oliguria GFR↓ distal sodium reabsorption retention of water & sodium blood volume ↑ edema hypertension Low serum complement
  • 16.
  • 17. typical manifEstation Develop acute nephritic syndrome 1–2 wk after an antecedent streptococcal pharyngitis or 3–6 wk after a streptococcal pyoderma. 1.Edema 75% of the patients Face, periorbital area  lower extremities  generalized (ascites, pleural effusions) 2. Proteinuria – usually normalize after 4 weeks 3. Oliguria school child < 400ml/day preschool child < 300ml/day infant & toddler < 200ml/day
  • 18. typical manifEstation 3. Gross hematuria (65% of patients) Smoky, tea-colored, cola-colored, or fresh bloody urine Microscopical hematuria (almost all patients) The urine appears normal, but >3 RBCs/HP are found in centrifuged urine sediment examined microscopically. 4. Hypertension (50%) – mild to moderate, typically subsides promptly after diuresis 5. Nonspecific symptoms: Such as anorexia, vomiting, general malaise, lethargy, abdominal or flank pain, low-grade fever and weight gain.
  • 19.
  • 20. Clinical course Spontaneous improvement typically begins within 1 wk with resolution of edema in 5-10 days and hypertension in 2-3 wk, but urinalysis may be abnormal (persistent microscopic hematuria) for a year.
  • 21. invEstigations Urinalysis and culture • Haematuria – present in all patients. • Proteinuria (trace to 2+, but may be in the nephrotic range; usually associated with more severe disease.) • Red blood cell casts (pathognomonic of acute glomerulonephritis). • Other cellular casts. • Pyuria may also be present.
  • 22. invEstigations  Bacteriological and serological evidence of antecedent streptococcal infection: • Raised ASOT ( > 200 IU/ml ). • Increased anti-DNAse B (if available) – a better serological marker of preceding streptococcal skin infection. • Throat swab or skin swab.  Renal function test • The BUN concentration is elevated in 75% of patients, and serum creatinine level is increased in one half of the patients, but profound decrease in GFR is uncommon in children. • Hyperkalemia, hypocalcaemia, hyponatremia, and metabolic acidosis are seen only in severe patients.
  • 23. InvestIgatIons  Full blood count • A mild normochromic anemia may be present from hemodilution and low-grade hemolysis. • Leucocytosis may be present.  Complement levels • C3 level – low at onset of symptoms, normalizes by 6wks • C4 is usually within normal limits in post-streptococcal AGN.  Ultrasound of the kidneys • Not necessary if patient has clear cut acute nephritic syndrome.
  • 24. IndIcatIons for renal BIopsy  Severe acute renal failure requiring dialysis.  Features suggesting non post-infectious AGN as the cause of acute nephritis.  Delayed resolution • Oliguria > 2 weeks • Azotaemia > 3 weeks • Gross haematuria > 3 weeks • Persistent proteinuria > 6 months
  • 25. lIght mIcroscope not specIfIc for post streptococcal nephrItIs •Glomeruli appear enlarged and hypercellular. •Diffuse mesangial cell proliferation with an increase in mesangial matrix. •Polymorphonuclear leukocytes are common in glomeruli during the early stage of the disease.
  • 26. dIagnosIs Acute onset Symptoms: edema, oliguria, dark urine, hypertension Urinalysis: RBCs, protein, casts Evidences of streptococcal infection: – Prodromes – Elavated serum titers of Abs to streptozymes(ASO) Serum C3 - Reduced
  • 29. management Strict monitoring - fluid intake, urine output, daily weight, BP (Nephrotic chart) Penicillin V for 10 days to eliminate β - haemolytic streptococcal infection (give erythromycin if penicillin is contraindicated) Fluid restriction to control oedema and circulatory overload during oliguric phase until child diureses and blood pressure is controlled
  • 30. management • Day 1 : up to 400 mls/m²/day. Do not administer intravenous or oral fluids if child has pulmonary oedema. • Day 2 : till patient diureses – 400 mls/m²/day (as long as patient remains in circulatory overload) • When child is in diuresis – free fluid is allowed Diuretic (e.g. Frusemide) should be given in children with pulmonary oedema. It is also usually needed for treatment of hypertension. Diet – no added salt to diet. Protein restriction is unnecessary
  • 31. complIcatIons Look out for complications of post- streptococcal AGN: • Hypertensive encephalopathy usually presenting with seizures • Pulmonary oedema (acute left ventricular failure) • Acute renal failure
  • 32. management for complIcatIons Significant asymptomatic hypertension symptomatic, severe hypertension or hypertensive emergency / encephalopathy
  • 33.
  • 34. Prehypertension is defined as a blood pressure in at least the 90th percentile, but less than the 95th percentile, for age, sex, and height, or a measurement of 120/80 mm Hg or greater. Hypertension is defined as blood pressure in the 95th percentile or greater.
  • 35.
  • 36. Acute pulmonary edema MANAGEMENT for coMplicATioNs
  • 38. follow-up  For at least 1 year. Monitor BP at every visit Do urinalysis and renal function to evaluate recovery. Repeat C3 levels 6 weeks later if not already normalised by the time of discharge.
  • 39. ouTcoME  Short term outcome: Excellent, mortality <0.5%.  Long term outcome: 1.8% of children develop chronic kidney disease following post streptococcal AGN.  These children should be referred to the paediatric nephrologists for further evaluation and management.
  • 40. sourcEs Paediatric Protocols 3rd Edition Nelson Textbook of Pediatrics, 7th Edition Renal Unit , Royal Hospital for Sick Children , Yorkhill Division © 2008 American Society of Nephrology

Notas del editor

  1. Normal histological structure of a glomerulus. On the right, is a 3-D illustration of a glomerulus. Left one shows AA = affrent arteriole, EA= Efferent arteriole, BC= Bowman’s capsule, US= Urinary space
  2. There is an overlap between these terms