Contrast-Induced Nephropathy: A Review Focusing on X-ray and CT Applications and the Iso-Osmolar Controversy

After administration of contrast media the incidence of acute renal failure requiring dialysis is low. Clinical studies on contrast-induced nephropathy (CIN) therefore use a relative or absolute increase in serum creatinine as a surrogate marker. However, there is no generally accepted threshold for increases in creatinine. The lack of consistency in the definition of CIN makes it difficult to compare trials. The serum creatinine level is also only a poor marker of renal function. Increases in serum creatinine after contrast examination are associated with increased mortality, morbidity and longer hospital stays. However, such correlations have been shown only for coronary interventions. Not all cases of renal failure following cardiac angiography are necessarily related to the contrast medium, as in these patients there are several other reasons for loss of renal function. There are no studies showing a correlation between patient outcome and CIN after intravenous administration of contrast media. While the pathophysiology of CIN is not yet completely understood, it most certainly involves the interplay of multiple factors. It is highly likely that direct tubular toxicity of the CM contributes to the aetiology, whereas the role of the physicochemical properties of CM may have been over-interpreted. There is an ongoing controversy as to whether the iso-osmolar CM iodixanol is better tolerated by the kidneys than low-osmolar CM (LOCM). Some randomized trials have demonstrated benefits of this substance. However, to date meta-analyses and registry studies have not shown a consistent picture. In the last few months some randomized trials have been published which have not found an advantage of iodixanol over LOMC, whether administered intra-arterially or intravenously.