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Richard E Katholi
American Heart Journal Volume 7 No.1

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Contrast-induced nephropathy (CIN) represents an increasing healthcare burden and challenge as the frequency of diagnostic imaging and interventional procedures increases, particularly among patients at risk for developing CIN. Universally accepted strategies to reduce the risk for CIN include careful patient screening and selection, adequate patient hydration, limiting the volume of contrast medium administered, and choosing a safe, non-ionic, low-osmolar contrast agent. For both intra-arterial and intravenous use, all ionic and non-ionic iodinated contrast agents may further impair renal function in high-risk patients. Based on comparisons of contrastmedia in proximal renal tubular cell culture and in recent robust head-to-head prospective clinical trials in high-risk patients, however, iso-osmolar iodixanol and low-osmolar iopamidol are comparable and appear to be the contrast agents of choice to reduce renal risk for CIN.

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Contrast-induced nephropathy (CIN) represents an increasing healthcare burden and challenge as the frequency of diagnostic imaging and interventional procedures increases, particularly among patients at risk for developing CIN. As the population ages, decreased renal function and increased atherosclerotic cardiovascular disease become more prevalent. An increasing incidence of obesity with resultant metabolic syndrome and/or adult diabetes also increases the population at risk for CIN.

Clinical Implications of Contrast-induced Nephropathy
CIN is the third most common cause of hospital-acquired acute renal failure.¹ The incidence of CIN is < 5% in patients with normal renal function and 15-50% in patients with renal dysfunction. The incidence of dialysis-dependent acute tubular necrosis is 1.3-19%. CIN is an indicator of a marked increase in short-term and late mortality.² Acute renal failure after coronary intervention is associated with a 36% in-hospital mortality rate and a 19% two-year survival rate.²

Strategies to Reduce the Risk for Contrast-induced Nephropathy
The pathogenesis of CIN is complex, with a cascade of contributing factors (see Figure 1). Besides CIN, there are other causes of acute renal dysfunction after angiography, including atheroemboli and hypotension.³ Examples of sudden hypotension during angiography include acute ST-elevation myocardial infarction and balloon dilatation during carotid stenting. At present, CIN cannot be prevented, but it can be attenuated.⁴ Universally accepted strategies to reduce the risk for CIN include careful patient screening and selection, adequate patient hydration, limiting the volume of contrast medium (CM) administered, and choosing a safe, non-ionic, lowosmolar contrast agent.⁵ In view of the clinical relationship between CIN and patient morbidity and mortality, identifying patients at risk and considering whether exposure to CM is necessary for diagnosis and/or intervention is implicit.

Recent guidelines have advocated routine use of the estimated glomerular filtration rate (eGFR) to identify patients with chronic kidney disease because serum creatinine is an insensitive measure of kidney dysfunction.⁶ Patients who are at particular risk for developing CIN include those with an eGFR < 60ml/min/1.73m2.³ All patients receiving CM should maintain adequate hydration. Intravenous volume expansion with isotonic saline (1.0-1.5ml/kg/h) for three to 12 hours before the procedure and continued for six to 24 hours has been shown to attenuate CIN.⁵

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