Acute kidney injury

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Background

  • An inability of the kidneys to maintain body homeostasis, usually defined by an acute increase in creatinine
  • Novel biomarkers are under development to complement creatinine, and are generally classified into:
    • Stress markers
    • Damage markers
    • Functional markers, including cystatin C

KDIGO Staging

Stage Serum Creatinine Urine Output
1 1.5 to 1.9 times baseline, or

≥26.5 μmol/L increase

<0.5 mL/kg/h for 6-12 hours
2 2 to 2.9 times baseline <0.5 mL/kg/h for ≥12 hours
3 3 times baseline, or ≥353.6 μmol/L, or started renal replacement therapy <0.3 mL/kg/h for ≥24 hours, or anuria for ≥12 hours

Differential Diagnosis

Clinical Manifestations

Clinical Clues of Etiology

Type History Examination
Prerenal Volume loss (e.g. vomiting, diarrhea, diuretics, hemorrhage, burns)
Thirst and reduced fluid intake
Heart failure or cirrhosis
Weight loss, orthostatic hypotension and tachycardiac, poor skin turgor, signs of heart failure or liver failure
Intrinsic renal ATN History of nephrotoxic medications, hypotension, trauma or myalgias suggestion rhabdo, CT contrast Muscle tenderness, compartment syndrome, volume status
GN Lupus, systemic sclerosis, rash, arthritis, uveitis, weight loss, fatigue, HCV infection, HIV infection, hematuria, foamy urine, cough, sinusitis, hemoptysis Periorbital, sacral, and lower-extremity edema; rash; oral or nasal ulcers
AIN Medication use (antiiotics, PPIs), rash, arthralgias, fever, infection Fever, drug rash
Vascular Nephrotic syndrome, trauma, flank pain, anticoagulation, vascular surgery Livedo reticularis, fundoscopy showing malignant hypertension, abdominal bruits
Post-renal Urinary urgency or hesitancy, gross hematuria, polyuria, stones, medications, cancer Bladder distension, pelvic mass, prostate enlargement

Source: Rahman M, Shad F, and Smith MC. Acute kidney injury: A guide to diagnosis and management. Am Fam Physician. 2012;86(7):631-639.

Investigations

  • Laboratory
    • Urinalysis and microscopy
      • Granular casts (from heme), suggesting ATN
      • Red blood cell casts, suggesting GN
    • Urine sodium
      • <10mmol/L suggests pre-renal, unless diuresed
    • Urea to creatinine ratio
      • Increased ratio suggests pre-renal cause
    • Extended electrolytes
  • Renal ultrasound, for possible obstruction

Fractional excretion of sodium (FENa)

$FENa = \frac{U_{Na} \div U_{Cr}}{S_{Na} \div S_{Cr}} = \frac{U_{Na} \times S_{Cr}}{S_{Na} \times U_{Cr}}$

FENa Etiology
<1% Pre-renal
1 to 4%
>2%
Intrinsic renal
Acute tubular necrosis (ATN)
>4% Post-obstructive

Management

  • Treatment depends on etiology
    • Prerenal: Fluid challenge
    • Renal: Stop nephrotoxic medications
    • Post-renal: Nephrostomy tubes
  • Dialysis if
    • Acidosis
    • Electrolyte imbalance (K+)
    • Intoxication (drugs, alcohols)
    • Overloaded fluid (heart failure)
    • Uremia (pericarditis, neurological symptoms)

Prognosis

  • Increased risk of developing CKD with
    • Increasing age
    • Female sex
    • AKIN stage
    • Absolute increase in serum creatinine
    • Albuminuria