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Contrast Nephropathy

by Navin Jaipaul, MD, MHS

Contrast nephropathy is worsening of renal function after IV administration of radiocontrast and is usually temporary. Diagnosis is based on a progressive rise in serum creatinine 24 to 48 h after contrast is given. Treatment is supportive. Volume loading with isotonic saline before and after contrast administration may help in prevention.

Contrast nephropathy is acute tubular necrosis (see Acute Tubular Necrosis (ATN)) caused by an iodinated radiocontrast agent, all of which are nephrotoxic. However, risk is lower with newer contrast agents, which are nonionic and have a lower osmolality than older agents, whose osmolality is about 1400 to 1800 mOsm/kg. For example, 2nd-generation, low-osmolal agents (eg, iohexol, iopamidol, ioxaglate) have an osmolality of about 500 to 850 mOsm/kg, which is still higher than blood osmolality. Iodixanol, the first of the even newer iso-osmolal agents, has an osmolality of 290 mOsm/kg, about equal to that of blood.

The precise mechanism of radiocontrast toxicity is unknown but is suspected to be some combination of renal vasoconstriction and direct cytotoxic effects, perhaps through formation of reactive O 2 species, causing acute tubular necrosis.

Risk factors

Risk factors for nephrotoxicity are the following:

  • Older age

  • Preexisting chronic kidney disease

  • Diabetes mellitus

  • Heart failure

  • Multiple myeloma

  • High doses (eg, > 100 mL) of a hyperosmolar contrast agent (eg, during percutaneous coronary interventions)

  • Factors that reduce renal perfusion, such as volume depletion or the concurrent use of NSAIDs, diuretics, or ACE inhibitors

  • Concurrent use of nephrotoxic drugs (eg, aminoglycosides)

  • Liver failure


Diagnosis is based on a progressive rise in serum creatinine 24 to 48 h after a contrast study. Most patients have no symptoms. Renal function typically later returns to normal.

After femoral artery catheterization, contrast nephropathy may be difficult to distinguish from renal atheroembolism. Factors that can suggest renal atheroemboli include the following:

  • Delay in onset of increased creatinine > 48 h after the procedure

  • Presence of other atheroembolic findings (eg, livedo reticularis of the lower extremities or bluish discoloration of the toes)

  • Persistently poor renal function that may deteriorate in a stepwise fashion

  • Transient eosinophilia or eosinophiluria and low complement levels (measured if atheroemboli are seriously considered)


Treatment is supportive.


Prevention involves avoiding contrast when possible (eg, not using CT to diagnose appendicitis) and, when contrast is necessary for patients with risk factors, using a nonionic agent with the lowest osmolality at a low dose. When contrast is given, mild volume expansion with isotonic saline (ie, 154 mEq/L) is ideal; 1 mL/kg/h is given beginning 6 to 12 h before contrast is given and continued for 6 to 12 h after the procedure. A NaHCO 3 solution may also be infused but has no proven advantage over normal saline. Nephrotoxic drugs are avoided before and after the procedure. Acetylcysteine is an antioxidant that is sometimes given but has no proven benefit; protocols vary, but acetylcysteine, 600 mg po bid the day before and the day of the procedure, may be given, combined with saline infusion. Volume expansion may be most helpful in patients with mild preexisting renal disease and exposure to a low dose of contrast. Volume expansion should be avoided in heart failure.

Periprocedural continuous venovenous hemofiltration has no proven benefit compared with other less invasive strategies in preventing acute kidney injury in patients who have chronic kidney disease and who require high doses of contrast and also is not practical. Therefore, this procedure is not recommended. Patients undergoing regular hemodialysis for end-stage renal disease who require contrast do not typically need supplementary, prophylactic hemodialysis after the procedure.

Key Points

  • Although most patients recover from use of iodinated radiocontrast without clinical consequences, all such radiocontrast is nephrotoxic.

  • Suspect contrast nephropathy if serum creatinine increases 24 to 48 h after a contrast study.

  • Decrease the risk of contrast nephropathy, particularly in patients at risk, by minimizing the use and volume of contrast and expanding volume when possible.

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