Cardiac angiography and coronary/vascular interventions utilising intravascular contrast agents (CA) are being widely performed in a growing number of elderly patients with multiple comorbidities. In spite of improvements in their chemical structure, CA still possess kidney toxicity and represent one of the main causes of contrast-induced nephropathy (CIN) and hospital-acquired renal failure. These iatrogenic clinical complications are associated with increased in-hospital and long-term morbidity and mortality. Development of CIN prevention strategies is ongoing, but efforts have been hampered by an incomplete understanding of CIN pathophysiology. The most popular theories include a combination of decreased renal medullary blood flow, resulting in medullary ischaemia, free radical formation, and a direct toxic effect on tubular cells. The definition of CIN includes absolute (>0.5mg/dL/ >44micromol/l) or relative (>25%) increase in serum creatinine at 48-72 hours after exposure to a CA compared to baseline serum creatinine values, when alternative explanations for renal impairment have been excluded. Although the risk of renal function impairment associated with radiological procedures is low (0.6-2.3%) in the general population, it may be very high (up to 50%) in some subsets, especially in patients with major risk factors such as advanced chronic kidney disease (CKD) and diabetes mellitus. Because no...
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