Contrast-induced acute kidney injury (CI-AKI) is one of the most widely discussed and debated topics in cardiovascular medicine. With increasing number of contrast-media- (CM-) enhanced imaging studies being performed and growing octogenarian population with significant comorbidities, incidence of CI-AKI remains high. In this review, pathophysiology of CI-AKI, its relationship with different types of CM, role of serum and urinary biomarkers for diagnosing CI-AKI, and various prophylactic strategies used for nephroprotection against CI-AKI are discussed in detail. 1. Contrast-Induced Nephropathy Contrast-induced acute kidney injury (CI-AKI) is one of the most widely discussed and debated topics in cardiovascular medicine. This is because an increasing number of individuals are exposed to iodinated contrast media (CM) during imaging-based investigations for either diagnostic or interventional purposes. The changing demographics of population especially increasing life expectancy has resulted in larger octogenarian population with comorbidities such as hypertension (HTN), diabetes mellitus (DM), and renal and cardiovascular disease, all of which predispose to renal impairment [1]. An increase in the incidence of CI-AKI is therefore not surprising. Thus, it is important that more attention is given in order to understand the aetiology of CI-AKI and devise novel diagnostic methods and formulate effective prophylactic and therapeutic regimens to reduce its incidence. 2. Problems of Definition of CI-AKI Previously CI-AKI was defined as a condition characterized by acute and reversible renal failure of varying severity in patients exposed to intravascular CM and in the absence of other risk factors responsible for the change in renal function [2]. However, there were many problems with this definition. Firstly, renal failure may not be reversible [3]; secondly, there is no agreed threshold change in renal function to define a case; and thirdly, the CM may not be the sole but rather contributory factor to the renal impairment for a given patient. The problems with defining CI-AKI have hampered attempts to quantify its true burden and have led to conflicting estimates of its importance [4–6]. It would therefore be better to define a “case” in terms of clinical outcomes such as the need for dialysis or other intervention, rather than by the occurrence of a specific decline in the renal function. Today, CI-AKI is widely defined as an absolute increase in serum creatinine (SCr) of 0.5？mg/dL (44？μmol/L) or a relative increase of 25% from the baseline value, assessed
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