Acute Kidney Injury

Snapshot

  • A 56-year-old man presents with lower abdominal pain. His symptoms have progressively worsened over the course of the day. Medical history is significant for benign prostatic hyperplasia on tamsulosin. His blood pressure is 144/106 mmHg (normally, his blood pressure is 120/80 mmHg). On physical examination he has bladder distension. Laboratory testing is significant for a creatinine of 2.4 mg/dL (last serum creatinine was 0.7 mg/dL.) (Post-renal acute kidney injury likely secondary to benign prostatic hyperplasia)

Introduction

  • Clinical definition
    • acute reduction in glomerular filtration rate (GFR)
      • recall that GFR represents the sum of the filtration rates of nephrons
        • therefore, GFR reflects functioning renal mass
  • Epidemiology
    • risk factors
      • hypertension
      • chronic kidney disease
      • dehydration and volume depletion
      • diabetes
      • chronic liver or lung disease
  • Etiology
    • prerenal causes
      • decreased renal perfusion (e.g., hemorrhage, congestive heart failure, and diuretic use)
    • intrarenal causes
      • acute tubular necrosis
        • ischemia and toxic causes
      • interstitial nephritis
      • glomerulonephritis
      • vasculitis
      • hemolytic uremic syndrome  
    • postrenal causes 
      • urinary flow obstruction (e.g., benign prostatic hyperplasia and nephrolithiasis)
  • Pathogenesis
    • based upcome etiology (look at etiology)
  • Prognosis
    • lower rates of recovery in patients > 65 years of age
  • increased risk of end-stage renal disease, chronic kidney disease, and mortality

Presentation

  • Symptoms
    • may be asymptomatic
    • oliguria
    • anuria
    • polyuria
    • confusion
  • Physical exam
    • hypertension
    • edema
  • decreased urine output

Imaging

  • Renal ultrasound
    • indication
      • initial imaging study for assessing acute kidney injury
        • can assess for renal size and hydronephrosis
  • to assess for postrenal obstruction

Studies

  • Labs
    • increase in serum creatinine by ≥ 0.3 mg/dL within 48 hours
    • blood urea nitrogen (BUN):creatinine ratio
    • urinalysis
      • dipstick
        • to assess for protein, glucose, leukocyte esterase, hemoglobin and myoglobin, and specific gravity
      • microscopy
        • for example
          • red dysmorphic cells suggests a glomerular etiology (e.g., glomerulonephritis)
          • muddy brown casts suggests tubular necrosis
          • white blood cell casts suggest pyelonephritis or acute interstitial nephritis
    • fractional excretion of Na+ (FeNa+)
      • if patient is on diuretics use FeUrea
    • urine osmolality and Na+
Studies To Assess For Prerenal, Intrarenal, and Postrenal Acute Kidney Injury (AKI)
StudiesPrerenal AKI  Intrarenal AKIPostrenal AKI
Urine osmolality (mOsm/kg)> 500< 350< 350
FeNa < 1%> 2%< 1% in mild cases> 2% in severe cases
Urine Na(mEq/L)< 20> 40> 40
Serum BUN/Cr> 20:1< 15:1Variable

Differential

  • Acute gastrointestinal bleeding
  • Rhabdomyolysis
  • Medication-induced impairment of creatinine secretion
    • cimetidine
    • trimethoprim
  • pyrimethamine

Treatment

  • Treatment is dependent on the etiology of AKI and its consequences
    • for example
      • a patient who is hyperkalemic and not responding to medical treatment should be dialyzed
  • a patient with a history of excessive fluid loss (e.g., diarrhea and vomiting) should be given intravenous fluid

Complications

  • Hyperkalemia
  • Metabolic acidosis
  • Uremic encephalopathy and platelet dysfunction
  • Anemia
  • Chronic kidney disease