Acute kidney injury

Definition

• An inability of the kidneys to maintain body homeostasis, usually defined by an acute increase in creatinine

AKIN Stage

Stage	Serum creatinine	Or, urine output
1	Creatinine increase ≥26.5 umol/L or 1.5-2 times baseline	<0.5ml/kg/h for 6h
2	Creatinine increase 2-3 times baseline	<0.5ml/kg/h for 12h
3	Creatinine increase >3 times baseline, or creatinine ≥354 umol/L increased by at least 44 umol/L, or need for dialysis	<0.3ml/kg/h for 24h

Differential Diagnosis

• Pre-renal: decreased renal perfusion
  • Hypovolemia
  • Blood loss
  • Shock
  • Sepsis
  • Heart failure
  • Vomiting and diarrhea
• Renal/intrinsic
  • Glomerulonephritis (GN): glomerular damage
    • Primary
      • Minimal change (in children)
      • Membranous (in adults)
      • Focal sclerosing (in HIV patients)
    • Secondary
      • Focal sclerosing or diffuse (in diabetic patients)
      • Lupus, multiple myeloma, and amyloidosis
  • Acute tubular necrosis (ATN): tubular damage
    • Ischemia from prerenal disease
    • Toxins
    • Drugs
      • Aminoglycosides
      • Amphotericin
      • Cisplatin
    • Pigments: hemoglobin, myoglobin
    • Proteins: immunoglobulin light chains (e.g. multiple myeloma)
    • Crystals
      • Uric acid
      • Acyclovir
      • Methotrexate
      • Indinavir
      • Oral sodium phosphate
    • Contrast-induced
  • Acute interstitial nephritis (AIN): interstitial damage
    • Allergic
      • Antibiotics: beta-lactams, sulfonamides
      • NSAID
      • PPI
    • Infective
      • Pyelonephritis
      • Legionellosis
    • Infiltration
      • Sarcoidosis
      • Lymphoma
      • Leukemia
    • Autoimmune
      • Sjögren syndrome
      • TINU syndrome
      • IgG4 disease
      • Systemic lupus erythematosus
    • Small vessel disease
      • Cholesterol emboli
      • Thrombotic microangiopathy
        • HUS/TTP
        • DIC
        • Preeclampsia
        • Anti-phospholipid syndrome (APS)
        • Malignant hypertension
        • Scleroderma renal crisis
• Post-renal (obstructive)
  • Bladder neck
    • BPH or prostate cancer (in men)
    • Cervical cancer (in women)
  • Neurogenic bladder
    • Anticholinergics
  • Ureteral (bilateral)
    • Malignancy
    • Lymphadenopathy
    • Retroperitoneal fibrosis
    • Nephrolithiasis

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