Contrast-Induced Nephropathy

Tadhg G. Gleeson; Sudi Bulugahapitiya

Disclosures

Am J Roentgenol. 2004;183(6) 

In This Article

Definition

Contrast-induced nephropathy has become a significant source of hospital morbidity and mortality with the ever-increasing use of iodinated contrast media in diagnostic imaging and interventional procedures such as angiography in high-risk patients. It is the third most common cause of hospital-acquired acute renal failure, after surgery and hypotension.[1] In this clinical setting, radiologists must develop an ability to recognize predisposing risk factors, to institute appropriate preprocedural prophylactic treatments, and to have a knowledge of the clinical presentation and subsequent management of the condition.

Several authors have published in-depth review articles: most notably Katzberg,[2] who performed a thorough review of urologic contrast agents and their potential effects, and Tublin et al.,[1] who published a review in 1998 of current concepts relating to contrast nephropathy. Although many of their concepts still hold true, we intended to concentrate on risk-factor analysis and an updated and comprehensive review of current prophylactic agents, areas that, to date, have not, to our knowledge, been fully addressed while also providing a general overview of the issues relating to contrast-induced nephropathy that may be relevant to the modern radiologist.

Contrast-induced nephropathy is most commonly defined as acute renal failure occurring within 48 hr of exposure to intravascular radiographic contrast material that is not attributable to other causes.[3] Ideally, the impairment of renal function should be measured by serial creatinine clearance, but because this step may be neither practical nor cost-effective in many centers, most of the literature describes the use of isolated measurements of serum creatinine levels, even though this parameter may be less sensitive at reflecting subtle early changes in renal function and may be slower to reach maximal sensitivity than creatinine clearance. Serum creatinine levels may prove to be more sensitive, however, in cases of preexisting renal impairment, in which tubular secretion of creatinine can lead to overestimation of the glomerular filtration rate (GFR).

An arbitrary range of values of between 25% and 50% (an increase in absolute values of 0.5–1.0 mg/dL) increase in serum creatinine levels from baseline has been suggested to define contrast-induced nephropathy.[2,4] Other suggested definitions include the following: a rise in serum creatinine levels of more than 100%, a rise in serum creatinine levels of more than 1 mg/dL, a postprocedural serum creatinine level greater than 5 mg/dL, or acute renal failure requiring dialysis.[5] Lautin et al.[6] used six separate definitions with criteria ranging from an increase in creatinine level of more than 0.3 mg/dL to an increase of 2.0 mg/dL or more and found the more restrictive higher cutoff point to be less sensitive for predicting incidences of contrast-related renal dysfunction. Although it has been argued that a low increment of change of serum creatinine levels may not be clinically important, this low increment allows studies of reasonable sample size.[3] In addition a large cohort study by Levy et al.[7] has shown that even apparently small decreases in renal function can lead to excessive mortality rates independent of other risk factors, and given that small rises in serum creatinine levels actually represent a significant drop in GFR, a definition set at the lower end of the accepted range has become the most commonly quoted. Hayman[8] has suggested that changes of 0.3 mg/dL are not statistically significant in many laboratories; hence contrast-induced nephropathy has become most commonly defined as "a 25% increase in serum creatinine concentration from the baseline value, or an absolute increase of at least 0.5 mg/dL (44.2 µmole/L), which appears within 48 hours after the administration of radiographic contrast media, and is maintained for 2–5 days".[9]

This definition may in part account for the large number of cases reported showing only transient elevations of serum creatinine levels or at least elevations that do not require dialysis. Although this large number has led to questioning of the clinical relevance of such rises, these subtle changes have been shown to be associated with significant morbidity rates[7] and, in addition, may help to identify those with borderline renal function who may be at risk of developing fulminant renal failure in the future.

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