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Acute Kidney Injury

Acute Kidney Injury

Acute Kidney Injury

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AKI: Definition & Staging - Kidney SOS Stages

  • Definition: Sudden ↓ kidney function: ↑ serum creatinine (sCr) & ↓ urine output (UO).
  • Staging (KDIGO-based / Kidney SOS adapted):
    • Stage 1:
      • sCr: ↑ ≥0.3 mg/dL (in 48h) OR 1.5-1.9x baseline
      • UO: < 0.5 mL/kg/hr for 6-12 hrs
    • Stage 2:
      • sCr: ↑ 2.0-2.9x baseline
      • UO: < 0.5 mL/kg/hr for ≥12 hrs

      ⭐ Oliguria in neonates is defined as urine output < 1 mL/kg/hr, and < 0.5 mL/kg/hr in older children.

    • Stage 3:
      • sCr: ↑ ≥3.0x baseline OR sCr ≥4.0 mg/dL OR RRT init.
      • UO: < 0.3 mL/kg/hr for ≥24 hrs OR Anuria ≥12 hrs

AKI: Etiology - Tiny Trouble Triggers

  • AKI arises from prerenal, intrinsic renal, or postrenal causes.
  • Prerenal (most common in children, ~70%):
    • ↓ Perfusion: Dehydration (diarrhea, vomiting), sepsis, shock, hemorrhage.
    • ↓ Effective volume: Heart failure, nephrotic syndrome.
  • Intrinsic Renal (~20%):
    • Acute Tubular Necrosis (ATN): Ischemia (prolonged prerenal), nephrotoxins (aminoglycosides, NSAIDs).
    • Glomerulonephritis (GN): PSGN, IgA nephropathy.
    • Hemolytic Uremic Syndrome (HUS). 📌 (D+ HUS: E.coli O157:H7)
    • Acute Interstitial Nephritis (AIN): Drugs, infections.
  • Postrenal (~5-10%):
    • Posterior Urethral Valves (PUV) in boys.
    • Stones, tumors, neurogenic bladder.

⭐ Hemolytic Uremic Syndrome (HUS) is a leading cause of intrinsic AKI in young children, often post-diarrheal (D+ HUS).

Pediatric AKI Causes: Prerenal, Intrinsic, Postrenal

AKI: Diagnosis - Spotting Sick Kidneys

Clinical Clues:

  • ↓UO: Oliguria (<0.5-1 mL/kg/hr), Anuria (<0.1 mL/kg/hr)
  • Edema, Hypertension
  • Hematuria, pallor, nausea

Key Investigations:

TestFinding
UO↓ (Oliguria/Anuria)
sCr/BUN↑ (sCr ↑ KDIGO: ≥0.3mg/dL or 1.5x baseline)
ElectrolytesK⁺↑, Na⁺↓, PO₄³⁻↑, Ca²⁺↓, Acidosis
UrinalysisCasts (muddy brown in ATN), proteinuria
FeNa$FeNa = \frac{U_{Na} \times P_{Cr}}{P_{Na} \times U_{Cr}} \times 100%$ (Prerenal <1%, Intrinsic >2%)
USG KUBObstruction, size, echotexture

AKI: Management & Complications - Fixing & Future Foes

  • General: Treat cause, optimize hemodynamics, avoid nephrotoxins, monitor I/O, weight.
  • Fluids: Euovolemia goal. Challenge: 10-20 mL/kg isotonic crystalloid if hypovolemic. Restrict if overloaded/oliguric.
  • Electrolytes:
    • Hyperkalemia (K+ > 6.5 mEq/L or ECG changes): Ca gluconate, Insulin-Dextrose, Salbutamol.
    • Acidosis (pH < 7.1): Bicarbonate (cautiously).
  • Complications: CKD, HTN, anemia.

⭐ Life-threatening hyperkalemia (K+ > 6.5 mEq/L with ECG changes) is a critical emergency in AKI requiring immediate intervention including calcium gluconate, insulin-glucose, and beta-agonists.

High‑Yield Points - ⚡ Biggest Takeaways

  • Prerenal azotemia (hypovolemia, sepsis) is the most common cause of pediatric AKI.
  • Oliguria is a key sign; non-oliguric AKI also occurs.
  • FeNa < 1% typically indicates prerenal AKI.
  • Urine microscopy is vital: muddy brown casts suggest Acute Tubular Necrosis (ATN).
  • Manage by treating cause, ensuring fluid balance, and correcting electrolytes.
  • Hemolytic Uremic Syndrome (HUS) is a major cause of intrinsic renal AKI.
  • Dialysis indications: AEIOU (Acidosis, Electrolytes, Intoxication, Overload, Uremia).

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