For decades, fear of “contrast-induced nephropathy” has led clinicians to delay or withhold contrast-enhanced computed tomography (CT) in emergency patients whose outcome depended on a rapid diagnosis, based on observational literature that lacked adequate non-contrast control groups. This review synthesises current evidence on the true risk of acute kidney injury (AKI) after intravenous iodinated contrast administration in the emergency department (ED) and proposes a practical, table-based approach for the front-line clinician, drawing on the guidelines of the European Society of Urogenital Radiology, the American College of Radiology and National Kidney Foundation consensus statement, the Kidney Disease: Improving Global Outcomes initiative, and the principal propensity-matched cohort studies and the PRESERVE randomised trial. The most methodologically robust propensity score-matched studies do not show a significant excess risk of AKI, dialysis, or mortality after intravenous contrast-enhanced CT in patients with an estimated glomerular filtration rate (eGFR) of 30 mL/min/1.73 m² or higher, compared with unenhanced CT in matched controls; risk remains uncertain, though probably not negligible, below this threshold or in the presence of established AKI — a reading reinforced by a large contemporary multicentre study finding significantly higher odds of AKI in this range. The term “contrast-induced nephropathy” has consequently given way to the causally more cautious “contrast-associated acute kidney injury” (CA-AKI). The PRESERVE trial showed no benefit of sodium bicarbonate over isotonic saline, nor of N-acetylcysteine over placebo, in patients at high cardiovascular risk undergoing angiography. In the unstable patient, or when the diagnosis under consideration is life- or organ-threatening, contrast administration should almost never be delayed to “wait for creatinine.” Rational prevention rests on targeted risk stratification, simple hydration in stable high-ri