Contrast-induced nephropathy following angiography and cardiac interventions

To cite: Rear R, Bell RM, Hausenloy DJ. Heart Published Online First: [please include Day Month Year] doi:10.1136/heartjnl2014-306962 INTRODUCTION Contrast-induced nephropathy (CIN), also known as contrast-induced acute kidney injury, is an iatrogenic renal injury that follows intravascular administration of radio-opaque contrast media (CM) in susceptible individuals. CIN was first described during the 1950s in case reports of fatal acute renal failure that had occurred following intravenous pyelography in patients with renal disease arising from multiple myeloma. 2 Despite technological advances, CIN remains responsible for a third of all hospital-acquired acute kidney injury (AKI) 4 and affects between 1% and 2% of the general population and up to 50% of high-risk subgroups following coronary angiography (CA) or percutaneous coronary intervention (PCI). The proliferation of imaging methods and interventional procedures involving administration of intravascular CM in both non-cardiac modalities (eg, vascular CT angiography and interventional vascular angiography) and in established (eg, CA and PCI) and emerging cardiac modalities (eg, CT coronary angiography (CTCA) and transcatheter aortic valve implantation (TAVI)) has significantly increased the number of patients exposed to CM and thus the number at risk of CIN. The widespread adoption of primary PCI for the treatment of acute myocardial infarction (AMI), despite significantly improving cardiovascular outcomes, has increased the incidence of CIN due to the inherent difficulties in rapidly assessing CIN risk, instigating prophylactic measures, attendant haemodynamic compromise and higher contrast volumes, all known risk factors for the development of CIN. Despite several therapeutic approaches, the rising age and incidence of comorbidity within the broad cohort of cardiac patients receiving CM has ensured that the prevention of CIN remains a significant clinical challenge. As will be discussed in the following sections, the estimated risk of an individual developing CIN can be calculated using known pre-existent clinical and periprocedural factors, which are consistent with the proposed pathological mechanisms of CIN. Pre-existent stage III chronic kidney disease (CKD), defined as an estimated glomerular filtration rate (eGFR)<60 mL/min/1.73 m for greater than 3 months, is the most commonly identified risk factor for CIN; however, CIN can occur in the absence of underlying CKD if a number of other risk factors are also present. Risk scoring systems have been developed from cohort studies 9 that have enabled clinicians to predict the likelihood of CIN occurrence and have allowed targeted use of preventative therapies. The wholly iatrogenic and predictable nature of CIN makes it a particularly well-suited area for ongoing cardiovascular and nephrology research, with focus on pathophysiological mechanisms as well as novel risk assessment, preventative, diagnostic and therapeutic measures.