Contrast-Induced Nephropathy (CIN)—more accurately termed contrast-associated acute kidney injury (CA-AKI)—is a form of acute kidney injury that occurs following exposure to iodinated contrast media used in diagnostic and interventional imaging procedures. With the widespread use of CT scans, angiography, and endovascular interventions in the UAE, CIN remains a clinically important and preventable cause of kidney injury, particularly among high-risk patients.

CIN typically presents as a sudden rise in serum creatinine within 24 to 72 hours after contrast exposure, in the absence of an alternative explanation for kidney dysfunction. While most cases are mild and reversible, severe CIN can result in prolonged hospitalization, need for renal replacement therapy, and increased long-term risk of chronic kidney disease.

The pathophysiology of CIN is multifactorial. Contrast agents cause renal vasoconstriction, leading to reduced blood flow in the renal medulla, an area already vulnerable to low oxygen tension. In addition, contrast media exert direct tubular toxicity, generate oxidative stress, and increase tubular workload. These combined effects result in tubular cell injury, impaired filtration, and transient or persistent decline in kidney function.

Patients at highest risk include those with pre-existing chronic kidney disease, diabetes mellitus, dehydration, heart failure, advanced age, anemia, and hypotension. Repeated contrast exposure within a short interval and use of high contrast volumes further increase risk. In hospitalized and critically ill patients, CIN often occurs in conjunction with other insults such as sepsis or hemodynamic instability.

Clinically, CIN is often asymptomatic and detected through routine monitoring of kidney function following contrast exposure. In more severe cases, patients may develop reduced urine output, fluid retention, electrolyte disturbances, and symptoms related to acute kidney failure. Because clinical symptoms may be subtle, proactive risk assessment and monitoring are essential.

Diagnosis is based on the temporal relationship between contrast exposure and deterioration in kidney function, supported by laboratory findings. Urinalysis is typically bland, and imaging is used primarily to exclude other causes of AKI. Differentiating CIN from other forms of intrinsic AKI is important, especially in complex hospitalized patients.

Management of CIN is largely preventive and supportive. The most effective strategy is adequate intravenous hydration before and after contrast administration, tailored to the patient’s cardiovascular status. Minimizing contrast volume, avoiding repeat exposures, and withholding nephrotoxic medications where possible significantly reduce risk. Once CIN develops, treatment focuses on optimizing fluid balance, monitoring electrolytes, and providing renal support as needed. Dialysis is rarely required but may be necessary in severe cases.

Most patients experience gradual recovery of kidney function within one to two weeks. However, those with underlying kidney disease may have incomplete recovery and increased susceptibility to future renal injury. Early nephrology involvement in high-risk patients improves prevention, early detection, and long-term outcomes.