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Acute glomerulonephritis

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Bacterial : Group A hemolytic streptococci. staphylococcus , Pneumococcus , Salmonella. Viral : Hepatitis B & C , Mononucleosis. B) GN of undetermined etiology : ... – PowerPoint PPT presentation

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Title: Acute glomerulonephritis


1
Acute
glomerulonephritis
  • By Deepa

2
  • Definition
  • Characterized by acute onset of
  • edema
  • hematuria
  • oliguria
  • hypertension
  • Impairment of renal function
  • facial edema

3
  • Causes
  • A) Post infectious
  • Bacterial Group A ß hemolytic streptococci
  • staphylococcus , Pneumococcus ,
  • Salmonella
  • Viral Hepatitis B C , Mononucleosis
  • B) GN of undetermined etiology
  • Membranoproliferative GN
  • Rapidly progressive GN

4
  • C) Collagen vascular diseases
  • SLE
  • Henoch Schonlein Syndrome
  • Polyarteritis Nodosa
  • D) IgA nephropathy
  • E) Familial Nephropathy Alport Syndrome
  • AGN following Streptococcal infection is the most
    common type in children

5
Post streptococcal GN
  • Follows infection of throat or skin with
  • Group A ß hemolytic streptococci (usually 1 4
    weeks)
  • Common strains 12 , 4 , 1 with Pharyngitis
  • Type 49 with Pyoderma
  • Mainly involves school age boys
  • IS an Immune Complex Disease.

6
  • The antibody formed against streptococcus
    combines with antigen and forms Immune complex
  • Immune complex deposition along the capillary
    wall
  • Active complement
  • Inflammatory changes
  • Glomerular injury

7
  • Pathology
  • on light microscopy
  • Glomeruli are enlarged , hypercellular ,
    ischemic capillary loops narrowed
  • Hypercellularity due to
  • Infiltration by leucocytes , both neutrophils
    monocytes
  • Proliferation of endothelial mesangial cells
  • In severe cases by crescent formation
  • Swelling of endothelial cells along with
    proliferation leucocytic infiltration
    obliterates the capillary lumen
  • There may be interstitial edema inflamation.
    Tubules often contain red cell casts

8
  • Immunofluorescence staining
  • Granular deposits of IgG , IgM , C3 along the
    capillary walls basement membrane
  • Electron Microscopy
  • Discrete, amorphous, electron dense deposits on
    the subepithelial side of capillary basement
    membrane often shows Lumpy deposits.

9
  • Clinical features
  • Rapid onset with puffiness around the eyes
    pedal edema
  • hematuria
  • hypertension
  • varying degree of oliguria
  • urine is smoky, cola-coloured
  • pleural effusion ascites uncommon
  • Atypical presentation
  • convulsions due to hypertensive encephaclopathy
  • left ventricular failure pulmonary edema
  • Acute renal failure

10
  • Laboratory findings
  • Urine examination
  • shows red blood cells (dysmorphic) and granular
    casts.
  • significant protienuria (1 to 2)
  • white cells indicative of glomerular
    inflammation
  • Hemodilution Normocytic normochromic anemia
  • ESR
  • Blood levels of urea creatinine elevated during
    early phase (return to normal within 2-3 weeks)
  • With continuing oliguria hyponatremia
    hyperkalemia

11
  • Chest X-ray
  • prominent vascular markings suggesting
    hypervolemia
  • mild cardiomegaly
  • pleural effusion
  • ASO titre
  • Anti hyaluronidase , anti deoxyribonuclease ,
    anti NADase (decrease in 4 to 6 weeks)
  • Total hemolytic complement (CM 50) C3 are
    reduced (returns to normal in 8 weeks)

12
  • A renal biopsy is indicated only in patients
    where clinical features are atypical
  • age of onset lt 2 yrs
  • pressure of systemic features including
    arthritis, skin rash, hepatosplenomegaly
  • absence of elevated ASO titre normal C3 levels
  • prior h/o renal disease
  • oliguria azotemia rapidly worsen or do not
    resolve with 2-3 weeks

13
  • Treatment
  • Mainly supportive
  • Diet
  • intake of protein (0.6 g/kg/body.wt/day) sodium,
    potasium should be restricted till blood urea
    urine output
  • fluid intake should be restricted to an amount
    equal to insensible losses 24 hr urine output
  • Weight
  • should be weighed daily
  • in severe oliguria should lose 0.5 body wt./day
    because of endogenous catabolism
  • oral or parentral penicillin if throat or skin
    culture reveal Group A streptococcus

14
  • Diuretics
  • if pulmonary edema iv frusemide 2-4 mg/kg
  • not indicated, since edema is rarely massive and
    gradually disappears with return of renal
    function
  • Control of BP is essential
  • Mild hypertension- restrict salt water intake
  • Atenolol, hydralazine or nifedipine are
    effective
  • malignant HT- iv Nitroprusside/ Labetalol

15
  • Prolonged oliguria
  • level of blood urea elctrolytes monitered
  • dialysis is required in children with
  • renal failure
  • prolonged oligoanuria
  • fluid overload
  • life threatening electrolyte disturbance
  • Left ventricular failure
  • HT controlled iv frusemid given
  • if immediate diuresis not seen step to
    initiate urgent dialysis
  • venesection with removal of 100-200 mi of blood
    or trying rotating torniquets to reduce
    venous return to the heart
  • respiratory support with positive end-expiratory
    pressure may be needed

16
  • Prognosis
  • Good prognosis in children
  • Loss of edema fall in BP in first week
  • Gross hematuria significant proteinuria
    disappears in two weeks.
  • Microscopic hematuria slight proteinuria may
    be present

17
Thank you.........
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