• primary PCI
• preconditioning
• stable angina
• NSTEMI
• STEMI
• acute coronary syndrome
• hypertrophic cardiomyopathy
• platelet and angioplas
• stents
• sudden cardiac death
• cardiomyopathy apical
• myocarditis
• diastolic dysfunction
• cardiomyopathy hypertrophic
• EBM
• coronary artery disease (CAD)
• renal disease

It is clear that the development of contrast-induced nephropathy (CIN) is both common and prognostically important in patients undergoing interventional cardiovascular procedures. CIN is now established as the third most common cause of hospital-acquired acute kidney injury (after surgery and hypotension).1 The expansion in the use of iodinated contrast media in both diagnostic and interventional procedures, in combination with an increasingly elderly infirm patient population, means that the incidence of CIN is likely to grow rapidly.

Several studies have shown that CIN is associated with increased morbidity and mortality, extended length of hospital stay and increased hospital costs.2–5 However, the key question remains whether CIN is just a marker of adverse cardiovascular, renal and procedural factors of no direct pathophysiological importance or a direct cause of increased mortality and morbidity. This is a difficult question to answer, but the paper by Wi et al published in Heart6 adds to the growing body of evidence that suggests CIN is a protagonist rather than a spectator in the adverse outcomes, and hence that we should increase our efforts to make the administration of iodinated contrast media safer for our patients.