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Contrast-induced nephropathy (CIN) is defined as a renal dysfunction that occurs after contrast administration. It is measured as either a 0.5 mg/dL increase in absolute serum creatinine value within 48-72 hours after intravenous contrast administration, or a 25% increase in serum (SCr) creatinine from baseline.

For renal insufficiency to be related to contrast administration, it should be acute and not related to any other identifiable cause of renal failure. After contrast administration, SCr levels peak between 2 and 5 days and usually return to normal in about 2 weeks.

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CIN is one of the leading causes of nosocomial acute kidney injury (AKI). It is associated with a higher risk of mortality, even in patients who do not undergo dialysis.

 

Prevention:

While the causality between Contrast Media (CM) application and AKI remains controversial, health workers should provide optimal individualized care in patients who have both potential risks and benefits from contrast-enhanced imaging studies or interventions. The official guidelines published by the American College of Radiology and the European Society of Urogenital Radiology both recommend prophylactic intravenous hydration (1.0–1.5 mL/kg/h) in patients at risk for AKI at least 6 hours before and after CM administration. Since CM are osmotic diuretics, they can cause the pre-renal effects of dehydration, a risk factor for AKI which can be reduced by optimal patient hydration. It has also been reported that intravenous hydration represents an effective preventive measure in patients at risk for CIN.  Consequently, it has been common to implement aggressive hydration protocols in the context of CM administration. However, the recent controversial discussion regarding the correlation of CM administration and AKI/CIN also questions the efficacy of such preventive measures. Concrete evidence for the appropriateness of hydration in patients undergoing contrast-enhanced imaging is still missing. There is a lack of randomized trials with adequate statistical power to prove the value of hydration for preventing CIN. Moreover, there is currently no official agreement on the value of other prophylactic measures such as antioxidant therapy (e.g., n-acetylcysteine and sodium bicarbonate) or vasodilators (to reverse medullary ischemia). Most data suggest that these measures are not effective. Thus, no preventive measures can be strongly recommended for current clinical practice, particularly in patients who could be harmed by rapid administration of intravenous fluids, like those with congestive heart failure.

 

When to Suspect and How to Treat:

Urinary epithelial cell casts, debris, and urate and calcium oxalate crystals are nonspecific findings in contrast-induced nephropathy. Low urinary sodium and fractional excretion of sodium (< 1%) have been reported as being distinctive characteristics of this condition, but these findings have not consistently been shown to be specific for contrast-induced nephropathy. A persistent nephrogram on radiography or CT 24 hr after contrast administration is also said to be suggestive of a diagnosis of contrast-induced nephropathy, but is not a consistent or a specific finding. Contrast-induced nephropathy most commonly manifests as a nonoliguric and asymptomatic transient decline in renal function. Oliguric acute renal failure requiring hemodialysis can occur. This condition presents with oliguria (24-hr urine volume < 400 mL) within 24 hr of contrast administration and typically persists for 2–5 days. Morbidity and mortality rates are significantly higher in this group of patients when compared with those who have nonoliguric renal failure. Treatment of established contrast-induced nephropathy should start with the recognition of renal impairment after the study. In patients at higher risk, renal function should be carefully monitored by measuring serum creatinine levels before and once daily for 5 days after the radiographic procedure. After contrast-induced nephropathy is identified, the subsequent management of this condition is the same as that for acute renal failure due to other causes. Admission to the hospital and subsequent monitoring of serum electrolyte levels are required to prevent hyperkalemia, hyponatremia, hyperphosphatemia, hypocalcemia, hypermagnesemia, and metabolic acidosis associated with acute renal failure. Appropriate nutritional support is essential and strict recording of patient weight and fluid input–output is required until creatinine levels return to baseline. High phosphate levels can be treated using phosphate binders such as calcium carbonate; hyperkalemia is treated by dietary restriction and potassium-binding resins or insulin–dextrose infusion when the potassium level is greater than 6.5 mmol/L. Correction of acidosis may require oral sodium bicarbonate. More severe cases may require temporary hemodialysis, but a minority.

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