Nephrology and Urology· Topic 9.1 Acute kidney injury and tubulointerstitial disease· 9.1.5

Contrast-induced nephropathy

Contrast-induced nephropathy is acute kidney injury directly mediated by iodinated contrast, a subset of the broader contrast-associated nephropathy that follows contrast exposure by 24 to 48 hours, occurring mainly in patients with reduced baseline eGFR. Prevention with periprocedural isotonic saline in high-risk patients and minimizing contrast volume is the mainstay, since treatment once it occurs is supportive.

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What this article covers

  • Overview

    Contrast-induced nephropathy (CIN) is acute kidney injury directly mediated by iodinated contrast, defined operationally as a rise in serum creatinine within 24 to 48 hours of contrast exposure that…

  • Epidemiology

    Risk rises with the severity of underlying CKD, and is concentrated in patients with an estimated glomerular filtration rate (eGFR) under 30 mL/min/1.73 m2 or with active AKI at the time of contrast exposure.

  • Risk factors

    Baseline eGFR <30 mL/min/1.73 m2, the single most important and best-established risk factor, especially when combined with active AKI.

  • Pathophysiology

    Direct tubular toxicity from the contrast agent, particularly with hyperosmolar formulations, injures proximal tubular epithelial cells and produces a pattern of acute tubular necrosis (ATN).

  • Clinical features

    Asymptomatic rise in serum creatinine beginning within 24 to 48 hours of contrast exposure is the typical presentation, often detected on routine postprocedure labs rather than through symptoms.

  • Differential diagnosis

    Acute tubular necrosis from another cause (sepsis, prolonged hypotension, aminoglycosides, other nephrotoxins): the discriminator is the absence of a contrast exposure in the preceding 24 to 48…

  • Diagnosis

    This is a clinical diagnosis, established first by a rise in serum creatinine within 24 to 48 hours of iodinated contrast exposure, in a patient without a more likely alternative explanation and with…

  • Management

    There is no specific treatment for established CIN; management is supportive, focused on avoiding further nephrotoxic insults while awaiting spontaneous recovery.

  • Complications

    Prolonged or worsened CKD, where CIN may accelerate progression toward a lower baseline eGFR even after apparent recovery.

  • Prognosis

    Usually reversible, with creatinine returning toward baseline within 1 to 3 weeks after a peak at 3 to 5 days in most patients.

  • Prevention

    Administer prophylactic IV 0.9% saline 1 mL/kg/hr, started 6-12 hours before the procedure and continued 6-12 hours after (reduced to 0.5 mL/kg/hr if ejection fraction is reduced), in all patients…

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