Contrast material (CM)-induced ne-phropathy (CIN) is the sudden rapid deterioration of renal func-tion that results from parenteral CM ad-ministration. This renal function deterio-ration has been variably defined as a min-imum increase from baseline serum creatinine (SCr) values of 25%-50% or an absolute increase in SCr of 0.5-1.0 mg/dL (1,2). The incidence of CIN has been reported to range from less than 1 % to greater than 30%. This wide variation in incidence is attributed to factors that include a lack of consensus in definitions, assessments based on SCr levels rather than more direct measures of kidney function, differing patient populations such as inpatients versus outpatients, wide variability in CM doses, variation in the completeness or timing of patient fol-low-up, and likely variation in the pa-tients hydration state. In addition, there has been a paucity of comparisons of the nephrotoxicity caused by CM adminis-tered by using different routes (eg, in-traarterial vs intravenous) (1-3).
CIN is not common in patients with normal preexisting renal function; rather, it is more frequent in patients with renal impairment, especially when the impairment is due to diabetic nephrop-athy (4). Even when both of these risk factors have been included, it has been difficult to establish an animal model reflective of the conditions in humans (5). This has hindered efforts to inves-tigate the pathogenesis of CIN and led some to question whether CIN even exists (6).
While there are numerous data on the incidence of CIN following cardiac angiography and intervention, the inci-dence of CIN after intravenous CM ad-ministration, particularly in high-risk patients, is less well established (7). Even less is known about the relative effect of using one CM versus another in terms of CIN following intravenous in-jection.
In this commentary, we assess evi-dence from clinical trials of the intrave-nous administration of CM, evidence derived from personal experience, and literature survey information to gain perspectives on the relative risk of CIN following intraarterial versus intrave-nous CM administration.