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ACUTE KIDNEY INJURY
IN PAEDIATRICS
CLM/M/0569/05/19
KIPTOO CHRISAR
AKI
It is the abrupt decrease in glomerular filtration rate (GFR) and tubular
function which may lead to decreased excretion of waste products.
This may lead to decreased excretion of waste products e.g. urea) and
disturbance in fluid and electrolyte homeostasis.
Epidemiology
• Occurs in 20 in 100,000 in neonates
• 2 in 100,000 in older children.
• Coexistence of AKI with critical illness occurs at the rate of 10% and
has 50% mortality in children requiring dialysis.
Etiology
• Pre renal
• Renal
• Post renal
Pre renal
• Also called pre renal azotemia.
• Characterized by diminished effective circulating arterial volume which
leads to inadequate renal perfusion and decrease in GFR.
• Reversible once the blood volume hemodynamic condition is restored to
normal
Causes
• Decreased true intravascular volume e.g. sepsis, burns haemorrhage and
acute gastroenteritis.
• Decreased effective intravascular volume e.g. anaphylaxis, cardiac failure,
shock and massive ascites.
Renal
• Obstruction of renal artery e.g. Renal vein thrombosis and Renal
arterial obstruction.
• Involvement of renal microvasculature
• Glomerular causes e.g. Crescentic glomerulonephritis.
• Interstitial causes e.g. acute tubulointerstitial nephritis
• Tubular causes e.g. Sepsis, snakebite,falcipurum malaria multiorgan
failure,SLE
Post renal
• Includes variety of disorders characterized by obstruction of the urinary
tract.
• Mostly bilateral.
• Relief of obstruction results in recovery of the renal function.
• Examples includes;
Tumours.
Ureterocele.
Haemorrhagic cystitis.
Neurogenic bladder.
CLINICAL MANIFESTATIONS
• Decreased or no urine output
• Fluid overload
• Hypertension
• Uraemia
A child with a hx of vomiting and diarrhoea is most likely itararuka

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Acute kidney injury in paediatrics

  • 1. ACUTE KIDNEY INJURY IN PAEDIATRICS CLM/M/0569/05/19 KIPTOO CHRISAR
  • 2. AKI It is the abrupt decrease in glomerular filtration rate (GFR) and tubular function which may lead to decreased excretion of waste products. This may lead to decreased excretion of waste products e.g. urea) and disturbance in fluid and electrolyte homeostasis.
  • 3. Epidemiology • Occurs in 20 in 100,000 in neonates • 2 in 100,000 in older children. • Coexistence of AKI with critical illness occurs at the rate of 10% and has 50% mortality in children requiring dialysis.
  • 4. Etiology • Pre renal • Renal • Post renal
  • 5. Pre renal • Also called pre renal azotemia. • Characterized by diminished effective circulating arterial volume which leads to inadequate renal perfusion and decrease in GFR. • Reversible once the blood volume hemodynamic condition is restored to normal Causes • Decreased true intravascular volume e.g. sepsis, burns haemorrhage and acute gastroenteritis. • Decreased effective intravascular volume e.g. anaphylaxis, cardiac failure, shock and massive ascites.
  • 6. Renal • Obstruction of renal artery e.g. Renal vein thrombosis and Renal arterial obstruction. • Involvement of renal microvasculature • Glomerular causes e.g. Crescentic glomerulonephritis. • Interstitial causes e.g. acute tubulointerstitial nephritis • Tubular causes e.g. Sepsis, snakebite,falcipurum malaria multiorgan failure,SLE
  • 7. Post renal • Includes variety of disorders characterized by obstruction of the urinary tract. • Mostly bilateral. • Relief of obstruction results in recovery of the renal function. • Examples includes; Tumours. Ureterocele. Haemorrhagic cystitis. Neurogenic bladder.
  • 8. CLINICAL MANIFESTATIONS • Decreased or no urine output • Fluid overload • Hypertension • Uraemia A child with a hx of vomiting and diarrhoea is most likely itararuka