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ACUTE GLOMERULONEPHRITIS
• Abrupt onset of hematuria
• Oliguria
• Edema
• Hypertension
ETIOLOGY
• 1)post infectious
• Strep,staph.hep BnC
• 2)Systemic vasculitis
• HSP,Wegener granulamatosis
• 3)others
• SLE,IgA nephropathy
Poststreptococcal GN
• AGN following group A hemolytic streptococci
• Infection of throat or skin precedes the onset
of nephritis by 1-4 wks
PATHOLOGY
• Light microscopy-proliferation of mesangial
cells and neutrophil infiltration
• Immunofluorescence-granular deposits of IgG
n complement C3
• Electron microscopy-deposits on subepithelial
side of GBM
Clinical Features
• School age children,males
Cola coloured urine
Puffiness around the eyes n pedal
edema
Oliguria
HTN
Mild proteinuria
Lab findings
• Urine-1-2+protein with redcells n
granular casts
• Hemodilution may result in normocytic
anemia
• ESR raised
• Blood urea n creatinine are elevated
• Hyponatremia n hyperkalemia
• ASO titre is increased
• Anti DNaseB is elevated
• Level of C3 is low
MANAGEMENT
• Mild oliguria n normal BP –managed at home
• 1)diet
• Restriction of Na K n fluids until blood urea
reduce n urine output increases
• 2)diuretics
• Oral furosemide at adose of 1-3mg/kg
• Pulmonary edema –IV frusimide 2-4 mg/kg
• 3)Hypertension
• Mild –restriction of salt n water intake
• amlodipine,nifedipine or diuretics
• 4)LV failure
• HTN should be controlled n IV
frusemide given to induce diuresis
• 5)prolonged oliguria
• Dialysis is indicated in children with
severe renal failure n prolonged
oligoanuria,fluid overload n life
threatening electrolytedisturbances
CRESCENTIC GN
• Rapidly progressive GN(RPGN)-a/c nephritic
illness accompanied by rapid loss of renal
function over days to wks
• Histopathology-crescents
• Management-initial administration of IV n oral
corticosteroids n IV cyclophosphamide followed
by maintenance immunosuppression
• Plasmapheresis in pauci-immune crescentic GN n
Goodpasture syndrome
NEPHRITIS IN HSP
• Most common vasculitis in children
• Microscopic hematuria n mild proteinuria
• Serum IgA levels elevate
• patient recover without any treatment
• Long term observation is necessary
IgA NEPHROPATHY
• Deposition of IgA in the glomeruli
• Recurrent episodes of gross hematuria
following URI
• Patient with hematuria n mild proteinuria-ACE
inhibitors
• Nephrotic range proteinuria or deranged renal
function –corticosteroids n alkylating agents
LUPUS NEPHRITIS
• Variable presentations
• Asymptomatic proteinuria,hematuria ,a/c
nephritic syndrome n neephrotic syndrome
• Mesangial n capillary wall deposits of IgG n
C3 n usually C1q n IgA
• Corticosteroids ,cytotoxic agents,calcineurin
inhibitors n monoclonal antibodies n
prompt treatment of infections has
improved outcomes

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Acute glomerulonephritis

  • 2. • Abrupt onset of hematuria • Oliguria • Edema • Hypertension
  • 3. ETIOLOGY • 1)post infectious • Strep,staph.hep BnC • 2)Systemic vasculitis • HSP,Wegener granulamatosis • 3)others • SLE,IgA nephropathy
  • 4. Poststreptococcal GN • AGN following group A hemolytic streptococci • Infection of throat or skin precedes the onset of nephritis by 1-4 wks
  • 5. PATHOLOGY • Light microscopy-proliferation of mesangial cells and neutrophil infiltration • Immunofluorescence-granular deposits of IgG n complement C3 • Electron microscopy-deposits on subepithelial side of GBM
  • 6. Clinical Features • School age children,males Cola coloured urine Puffiness around the eyes n pedal edema Oliguria HTN Mild proteinuria
  • 7. Lab findings • Urine-1-2+protein with redcells n granular casts • Hemodilution may result in normocytic anemia • ESR raised • Blood urea n creatinine are elevated • Hyponatremia n hyperkalemia
  • 8. • ASO titre is increased • Anti DNaseB is elevated • Level of C3 is low
  • 9. MANAGEMENT • Mild oliguria n normal BP –managed at home • 1)diet • Restriction of Na K n fluids until blood urea reduce n urine output increases • 2)diuretics • Oral furosemide at adose of 1-3mg/kg • Pulmonary edema –IV frusimide 2-4 mg/kg
  • 10. • 3)Hypertension • Mild –restriction of salt n water intake • amlodipine,nifedipine or diuretics • 4)LV failure • HTN should be controlled n IV frusemide given to induce diuresis
  • 11. • 5)prolonged oliguria • Dialysis is indicated in children with severe renal failure n prolonged oligoanuria,fluid overload n life threatening electrolytedisturbances
  • 12. CRESCENTIC GN • Rapidly progressive GN(RPGN)-a/c nephritic illness accompanied by rapid loss of renal function over days to wks • Histopathology-crescents • Management-initial administration of IV n oral corticosteroids n IV cyclophosphamide followed by maintenance immunosuppression • Plasmapheresis in pauci-immune crescentic GN n Goodpasture syndrome
  • 13. NEPHRITIS IN HSP • Most common vasculitis in children • Microscopic hematuria n mild proteinuria • Serum IgA levels elevate • patient recover without any treatment • Long term observation is necessary
  • 14. IgA NEPHROPATHY • Deposition of IgA in the glomeruli • Recurrent episodes of gross hematuria following URI • Patient with hematuria n mild proteinuria-ACE inhibitors • Nephrotic range proteinuria or deranged renal function –corticosteroids n alkylating agents
  • 15. LUPUS NEPHRITIS • Variable presentations • Asymptomatic proteinuria,hematuria ,a/c nephritic syndrome n neephrotic syndrome • Mesangial n capillary wall deposits of IgG n C3 n usually C1q n IgA • Corticosteroids ,cytotoxic agents,calcineurin inhibitors n monoclonal antibodies n prompt treatment of infections has improved outcomes