**3. Epidemiology**

CIN is one of the most significant causes of hospital-acquired acute kidney injury (AKI) [8] and presents about 12% of the cases [9]. It represents the third most common cause after renal hypoperfusion (42%) and postoperative renal injury (18%). The reported incidence of CIN following percutaneous coronary intervention (PCI) lies between 0 and 24%. This depends on the associated risk factors, with the greatest incidence being reported after emergency PCI [10, 11]. A meta-analysis which included 40 studies showed a 6% incidence of CIN following contrast-enhanced computed tomography (CT) [12], 9% following peripheral angiography [3], and 4% following intravenous pyelography [13]. The incidence of CIN is low in patients with normal renal function (0–5%) [14]. However, there is an incidence of 12–27% in patients having preexisting renal impairment [15]. Moreover, in one study, an incidence as high as 50% was found in patients with diabetic nephropathy undergoing coronary angiography despite the use of low-osmolar CM (LOCM) and adequate hydration. Also, up to 15% of them needed dialysis [16]. Development of CIN is associated with a longer duration of hospital stay and an increased morbidity and mortality, in addition to more costs [1, 17]. Elevation of post-PCI serum creatinine may have prognostic significance regardless of the initial kidney functions. In fact, a slight elevation in serum creatinine (25–35 μmol/l) is associated with an increase in 30-day mortality [18]. Furthermore, post-PCI serum creatinine elevation has been reported to be linked to higher 1-year mortality than periprocedural myocardial necrosis [19].
