AGN, beth

Acute Glomerulonephritis
Anatomy & physiology

 The glomerular network of specialized capillaries serves
as the filtering mechanism of the kidney.
 The glomerular capillaries are lined by endothelial cells
 The glomerular basement membrane (GBM) forms a

continuous layer between the endothelial and mesangial
cells on one side and the epithelial cells on the other.
Background
 AGN is characterized by the sudden appearance of
proteinuria, hematuria,red blood cell casts in the urine,
edema, and, hypertension with or without oliguria.
 Acute post streptococcal glomerulonephritis is one of the
most common glomerular causes of gross hematuria in
children, and it is a classic example of acute nephritic
syndrome
Common cause of gross hematuria
-Urinary tract infection
-Meatal stenosis
-Perineal irritation
-Trauma
-Urolithiasis
-Hypercalciuria
-Obstruction
-Coagulopathy
-Tumor
-Glomerular disease
-Post infectious glomerulonephritis
-Henoch-Schönlein purpura nephritis
-IgA nephropathy
-Alport syndrome (hereditary nephritis)
-Thin glomerular basement membrane disease
-Systemic lupus erythematosus nephritis
Etiologies
 Group A beta- hemolytic streptococcus(single most common)
 coagulase-positive and coagulase-negative staphylococci
 Streptococcus pneumoniae
 gram-negative bacteria
 Bacterial endocarditis
 fungal
 rickettsia
 viral diseases, particularly influenza

Etiology and Epidemiology
• Following Group A Beta hemolytic Streptococcus

throat or skin infection:
After throat Infection- 1-2 weeks,
-Temperate climate
-Early school age
After skin infection- 3-6 week
- Tropical
- Preschool
Pathophysiology
 PSGN follows infection with only certain strains of
streptococci designated as nephritogenic.
 Acute post streptococcal glomerulonephritis (APSGN) follows
pyoderma with streptococci M types 47, 49, 55, 2, 60, and 57
and throat infection with streptococci M types 1, 2, 4, 3, 25,
49, and 12.
 APSGN is believed to be an immune-mediated disease, in
which an immune complex containing a streptococcal antigen
is deposited in the affected glomeruli.
Cont..
Proposed mechanisms are:-
deposition of circulating immune complex
in situ glomerular immune complex ( molecular
mimiciry )
Cont..
 Light microscopy
 The kidneys appear symmetrically enlarged.
 All glomeruli appear enlarged and relatively bloodless and show

diffuse mesangial cell proliferation with an increase in mesangial
matrix .
 Polymorph nuclear leukocytes are common in glomeruli during the
early stage of the disease
 Crescents and interstitial inflammation may be seen in severe cases
Cont..
 Immunofluorescence microscopy: reveals lumpy-bumpy
deposits of immunoglobulin and complement on the GBM and
in the mesangium.
 Electron microscopy: electron-dense deposits, or “humps,”
are observed on the epithelial side of the GBM .
Clinical manifestation
 APSGN is most common in children aged 5–12 yr and is
uncommon before the age of 3 yr.
 Recent history of pharyngitis, tonsillitis, or pyoderma.
 Latent period
-1-2 weeks after a throat infection and

-3-6 weeks after a skin infection.
severity varies from asymptomatic to microscopic
hematuria to full blown nephritic syndrome
Cont..
 Oliguria
-This is present in 10-50% of cases, and, in 15%, urine output is

less than 200 mL.
-Oliguria is indicative of the severe crescentic form of the

disease.
-It is often transient, with diuresis occurring within 1-2 weeks.

 Hematuria
-caused by hemolysis of red blood cells that have penetrated the

glomerular basement membrane and have passed into the tubular
system
Cont..
 Edema
-Edema is present in 80-90% of cases, and it is the presenting

complaint in 60% of cases.
-Compromised intra-glomerular blood flow due to glomerular
hyper cellularity results in progressive encroachment on the
cross-sectional area of the glomerular capillaries.
-This leads to reduced blood flow that manifests as low
fractional excretion of sodium and concentrated urine. This
salt and water retention leads to edema.
Cont..
 Hypertension
-occurs in 60-80% of cases and is more common among elderly

individuals.
-In 50% of cases, the hypertension can be severe; however, more
often it is transient, with normalization of blood pressure upon
restoration of the glomerular filtration rate, loss of edema, and
normalization of plasma volume.
 Hypertensive encephalopathy occurs in no more than 5-10%
of patients. Usually, clinical improvement occurs without any
neurological sequelae
Diagnosis
 Urinalysis : shows red blood cells (RBCs), RBC casts,
proteinuria, and polymorph nuclear leukocytes.
 Low HCT: A mild normochromic anemia caused by
hemodilution and low-grade hemolysis.
 Low C3 level
 Elevated ASO titer
 anti-(DNase) B level
 Throat culture
 Brain MRI posterior reversible encephalopathy syndrome

 Renal biopsy: should be considered only in the
presence of acute renal failure, nephrotic syndrome,
absence of evidence of streptococcal infection, or
normal complement levels.
 In addition, renal biopsy is considered when hematuria
and proteinuria, diminished renal function, and/or a
low C3 level persist more than 2 mo after onset.
Differential diagnosis
 IGA nephropathy
 Good pasture syndrome
 Idiopathic rapidly progressive glomerulonephritis
Complications
 Acute complications result from hypertension and acute renal
dysfunction
- Hypertensive encephalopathy
- Heart failure
- Hyperkalemia,
- Hyperphosphatemia,
- Hypocalcemia,
- Acidosis,
- seizures, and uremia.
Treatment
• Management is directed at treating the acute effects of renal
insufficiency and hypertension
 Treatment of hypertension
 Sodium restriction,
 diuresis with intravenous Lasix
 pharmacotherapy -CCB, vasodilators, or ACE inhibitors.
• Systemic antibiotic therapy with penicillin for 10 days is

recommended to limit the spread of the nephritogenic
organisms, but does not affect the natural history of
glomerulonephritis
Outpatient care
 Follow up at 0-6 weeks as necessary to determine the
following:
- hypertension ,edema and gross hematuria
 Follow up 6-10 weeks
- azotemia has subsided
-anemia has subsided
-hypertension has resolved
-C3 and C4 levels have returned to normal
 Follow up at 3mo,6 mo & 9 mo
-hematuria and proteinuria are subsiding gradually
-BP is normal
 At 12 months
-proteinuria and microscopic hematuria has disappeared
Prognosis
 Acute phase generally resolve with in 6-8wks. Although urinary

protein excretion and HTN normalize by 4-6wks, persistent
microscopic hematuria can persist for 1-2yrs
 Complete recovery occurs in more than 95% of children with
acute post streptococcal glomerulonephritis.
 Chronic Renal Disease in <2% of affected children
 Recurrences are extremely rare(b/c of long-term persistence of

antibodies to nephritis-associated streptococcal antigen)
Thank You

AGN, beth

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Acute Glomerulonephritis

Anatomy & physiology

 The glomerular basement membrane (GBM) forms a

 coagulase-positive and coagulase-negative staphylococci

 viral diseases, particularly influenza

• Following Group A Beta hemolytic Streptococcus

 The kidneys appear symmetrically enlarged.

 All glomeruli appear enlarged and relatively bloodless and show

-1-2 weeks after a throat infection and

-This is present in 10-50% of cases, and, in 15%, urine output is

-Oliguria is indicative of the severe crescentic form of the

-It is often transient, with diuresis occurring within 1-2 weeks.

-caused by hemolysis of red blood cells that have penetrated the

-Edema is present in 80-90% of cases, and it is the presenting

-occurs in 60-80% of cases and is more common among elderly

 Elevated ASO titer

 Brain MRI posterior reversible encephalopathy syndrome

• Systemic antibiotic therapy with penicillin for 10 days is

 Acute phase generally resolve with in 6-8wks. Although urinary

 Recurrences are extremely rare(b/c of long-term persistence of

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