Kidney Injury, Acute

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Basics

Description

  • “Renal failure” is an outdated term
  • Acute kidney injury (AKI) is newly defined by the Kidney Disease Improving Global Outcomes (KDIGO) classification as:
    • Serum creatinine ≥0.3 mg/dL within 48 hr; or
    • Serum creatinine increase to ≥1.5 times baseline, occurring within prior 7 d; or
    • Urine volume <0.5 mL/kg/hr for 6 hr
  • Serum creatinine or urine volume maximum changes determine AKI stage
  • KDIGO staging:
    • Stage 1: Cr ≥0.3 mg/dL increase or 1.5–1.9 × baseline or UO <0.5 mg/kg/hr × 6 hr
    • Stage 2: Cr 2–2.9 × baseline or UO 0.5 mg/kg/hr × 12 hr
    • Stage 3: Cr ≥3 × baseline or ≥4 mg/dL or UO <0.3 mg/kg/hr × 24 hr or anuria ≥12 hr or the initiation of renal replacement therapy
  • AKI consequences include:
    • Waste product accumulation
    • Electrolyte disturbances
    • Fluid accumulation
    • Reduced immunity
    • Other organ dysfunction
  • AKI leads to increased morbidity and mortality
  • AKI biomarkers will become increasingly important for early diagnosis, differential diagnosis, and prognosis

Etiology

  • Prerenal AKI:
    • Caused by renal hypoperfusion
    • Renal tissue remains normal unless severe/prolonged hypoperfusion
  • Intrarenal AKI:
    • Caused by renal parenchymal diseases
  • Iatrogenic AKI, causes include:
    • Aminoglycoside antibiotics
    • NSAIDs
    • ACE inhibitors
    • Angiotensin receptor blockers
    • IV contrast may be a risk in patients with significant preexisting disease
  • Postrenal AKI:
    • Due to urinary tract obstruction (e.g., prostatic hypertrophy, prostatitis)

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Basics

Description

  • “Renal failure” is an outdated term
  • Acute kidney injury (AKI) is newly defined by the Kidney Disease Improving Global Outcomes (KDIGO) classification as:
    • Serum creatinine ≥0.3 mg/dL within 48 hr; or
    • Serum creatinine increase to ≥1.5 times baseline, occurring within prior 7 d; or
    • Urine volume <0.5 mL/kg/hr for 6 hr
  • Serum creatinine or urine volume maximum changes determine AKI stage
  • KDIGO staging:
    • Stage 1: Cr ≥0.3 mg/dL increase or 1.5–1.9 × baseline or UO <0.5 mg/kg/hr × 6 hr
    • Stage 2: Cr 2–2.9 × baseline or UO 0.5 mg/kg/hr × 12 hr
    • Stage 3: Cr ≥3 × baseline or ≥4 mg/dL or UO <0.3 mg/kg/hr × 24 hr or anuria ≥12 hr or the initiation of renal replacement therapy
  • AKI consequences include:
    • Waste product accumulation
    • Electrolyte disturbances
    • Fluid accumulation
    • Reduced immunity
    • Other organ dysfunction
  • AKI leads to increased morbidity and mortality
  • AKI biomarkers will become increasingly important for early diagnosis, differential diagnosis, and prognosis

Etiology

  • Prerenal AKI:
    • Caused by renal hypoperfusion
    • Renal tissue remains normal unless severe/prolonged hypoperfusion
  • Intrarenal AKI:
    • Caused by renal parenchymal diseases
  • Iatrogenic AKI, causes include:
    • Aminoglycoside antibiotics
    • NSAIDs
    • ACE inhibitors
    • Angiotensin receptor blockers
    • IV contrast may be a risk in patients with significant preexisting disease
  • Postrenal AKI:
    • Due to urinary tract obstruction (e.g., prostatic hypertrophy, prostatitis)

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