Contrast-induced acute kidney injury

Contrast-induced nephropathy (CIN) is described as a sudden deterioration of renal function i.e. an increase in serum creatinine (SCr) > 25% or an absolute rise of 0.5 mg/dL over a baseline in SCr within 48 hours of intravascular contrast administration in the absence of an alternative cause in absence of any other cause. The CIN has been reported as third most common cause of acute kidney injury in hospitalized patients. The exact mechanism of nephrotoxicity due to contrast agents is not yet clear yet it is presumed to be interplay renal vasoconstriction resulting in medullary hypoxemia and the direct cytotoxic effects of contrast agents on renal tubular cells. Diabetes, multiple myeloma, and advanced age are some of the modifiable factors while contrast volume, shock, hypotension, and congestive heart failure are a few non-modifiable risk factors for its occurance. Use of an imperfect marker of kidney function (SCr) may result in a false sense of safety, as only the ‘tip of the iceberg’ is being exposed by such measurements. Use of intravenous normal saline, sodium bicarbonate infusion and N-acetylcysteine are relatively cost-effective and safe, in reducing the risk of CIN, and may considered in patients undergoing procedures with intravascular contrast.