The administration of radiocontrast media can lead to a usually reversible form of acute kidney injury (AKI) that begins soon after the contrast is administered [1-11]. In most cases, there are no permanent sequelae, but there is some evidence that its development is associated with adverse outcomes .
This topic will provide an overview of the relative nephrotoxicity of different iodinated radiocontrast agents and the relative efficacy of various prophylactic strategies. The pathogenesis, clinical features, and diagnosis of radiocontrast media-induced nephropathy, and a discussion of acute tubular necrosis, the most common cause of AKI in hospitalized patients, are presented separately. (See "Pathogenesis, clinical features, and diagnosis of contrast-induced nephropathy" and "Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury (acute renal failure)" and "Renal and patient outcomes after acute tubular necrosis".)
Types of radiocontrast agents — Iodinated radiocontrast agents are either ionic or nonionic and, at the concentrations required for arteriography or computed tomography (CT), are of variable osmolality [10,13]:
●First-generation agents are ionic monomers; they are highly hyperosmolal (approximately 1400 to 1800 mosmol/kg), compared with the osmolality of plasma.
●Second-generation agents, such as iohexol, are nonionic monomers with a lower osmolality than the first-generation radiocontrast media; however, they still have an increased osmolality (500 to 850 mosmol/kg), compared with plasma. In addition, there is an ionic low-osmolal contrast agent (ioxaglate).