Updated: 12/1/2021

Contrast-Induced Nephropathy

Review Topic
  • Snapshot
    • A 78-year-old man underwent coronary angiography after a positive stress test. Approximately 48 hours after angiography, routine serum labs were significant for an increased creatine about 50% above baseline. He reports no change in urinary frequency or volume. Medical history is significant for coronary artery disease, chronic kidney disease, and type II diabetes mellitus. Physical examination is unchanged since before the procedure.
  • Introduction
    • Clinical definition
      • acute kidney injury soon (24-48 hours) after contrast media administration
  • Epidemiology
    • Incidence
      • dependent on the presence or absence of risk factors
      • among patients with no risk factors, the risk of contrast nephropathy is less than 1%
    • Risk factors
      • primary chronic kidney disease
      • diabetic nephropathy with renal insufficiency
      • multiple myeloma
      • contrast amount
      • causes of decreased renal perfusion (e.g., hypovolemia)
  • Etiology
    • Pathogenesis
      • contrast media results in acute tubular necrosis via unknown mechanisms
  • Presentation
    • Physical exam
      • oliguria (rare)
        • most patients are non-oliguric
  • Studies
    • Labs
      • serum creatinine
        • increased serum creatine within
          • 1-2 days after contrast administration
      • urinalysis
        • may show evidence of acute tubular necrosis such as
          • muddy brown granular casts
          • epithelial cellular casts
  • Differential
    • Ischemic acute tubular necrosis
    • Acute interstial nephritis
    • Renal atheroemboli
    • Acute kidney injury after angiography which
      • can be distinguished from contrast-induced nephropathy by
        • kidney injury occuring days to weeks after angiography
        • little or no recovery in renal function (frequently)
        • other embolic lesions or livedo reticularis
  • Treatment
    • Conservative
      • prevention
        • indication
          • there is no specific therapy for contrast-induced nephropathy and thus
            • prevention is the best treatment
        • modality
          • using other imaging modalities that do not require contrast if clinically possible
          • using decreased doses of contrast
          • avoiding renotoxic medications and volume depletion
          • intravenous isotonic fluids (e.g., normal saline or sodium bicarbonate)
      • supportive treatment
        • indication
          • in patients that develop acute kidney injury after contrast administration
        • modality
          • regularly monitoring electrolytes, BUN, and creatinine
          • management is similar to acute kiney injury from other causes
  • Complications
    • Residul renal dysfunction
  • Prognosis
    • In the majority of cases
      • over the course of a few days-to-one week the creatine returns to baseline (or close to it)
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