George M. Ebert, MD, PhD

The incidence of contrast-induced nephropathy (CIN) varies from 5% to 38%, depending on the risk factors that apply to the patient.1 To put this in perspective, an imaging center with one CT scanner scanning 10,000 patients a year using contrast in half the examinations would be putting 200 to 2,000 patients at risk for CIN. This percentage range probably comes as a surprise to many radiologists; because they rarely see patients once a diagnostic scan has been completed, they are unlikely ever to see the renal damage that can occur following contrast-enhanced examinations.

In fact, the only types of adverse reactions to contrast media that radiologists encounter tend to be cases of anaphylactic response, cardiac dysrhythmia and arrest, or cardiovascular and pulmonary collapse. If these serious events happen, they will occur almost instantly after the patient receives a dose of the contrast medium, causing hives, shortness of breath, loss of airway patency, or even cardiac arrest. Fortunately, while such reactions can be fatal, they are also uncommon. A clinic with a single scanner will probably encounter only one severe near-fatal reaction every 5 years.

In comparison, CIN occurs with much greater frequency and is more insidious, with effects that may not be visible for days or weeks after the diagnostic examination. Patients cannot even be prepared to monitor themselves for signs that CIN is imminent because, by the time that outward symptoms of renal failure are apparent, there is already significant kidney injury. Patients can lose 75% of kidney function and still appear healthy.

In some cases, CIN is temporary, with patients experiencing a transient elevation in their creatinine levels that can be completely resolved (unless they undergo additional diagnostic scanning within days). Without knowing how damaging contrast administration was for such patients, radiologists are unwittingly exposing them to further injury.

Most patients have no problems at all with contrast media, and permanent renal damage is rare even in those who do experience CIN. The condition can, however, prolong the patient’s hospital stay and increase the risk of nonrenal complications. Clearly, radiologists not only need to be aware of the potential for CIN, but must be prepared to reduce the likelihood of its occurrence.

Recognizing High-Risk Patients

Contrast-induced acute renal failure is defined as a creatinine level increased at least 0.5 mg/dL, or more than 25%, above the baseline level. Renal failure usually peaks within 3 to 5 days after completion of the diagnostic procedure and is most often self-limiting.2 Contrast agents cause nephropathy primarily through renal ischemia and, possibly, through direct toxicity to tubular epithelial cells. After contrast is injected, renal blood flow transiently increases; it then decreases over a longer time, suggesting that renal ischemia is a major factor in the pathogenesis of CIN.3

Preexisting renal insufficiency is the single greatest risk factor for CIN, occurring in an estimated 60% of patients with CIN. The more severe the baseline renal insufficiency, the greater the risk that a patient will develop CIN.4

Consequently, radiologists need to be aware of underlying disease states, particularly diabetes and impaired cardiac function, in their patients. Patients with diabetes and pre-existing renal insufficiency have a greater risk of CIN than nondiabetic patients with similar levels of pre-existing renal insufficiency. Moreover, when patients in this high-risk group develop nephropathy, they more often develop oliguria and need dialysis.5

In screening for potential contrast-related problems, the simplest approach (for both inpatients and outpatients) is to check blood urea nitrogen and creatinine levels prior to performing a scan. Although the risk of CIN associated with a given serum creatinine value can vary widely, a rough estimate of the risk (as a percentage) can be obtained by multiplying the serum creatinine concentration (mg/dL) by 10.2 Determining this level in advance is, essentially, cheap insurance for a patient’s kidneys, and this step will give the radiologist valuable information about the safety of contrast use.

Whereas a radiology department within a hospital may have the ability to order an immediate assessment of the patient’s creatinine level to determine the risk of CIN, this is unlikely to be an option at an imaging center that is not associated with a hospital. Ideally, a center that is unable to run this test would, when in doubt, delay a patient’s scan until the creatinine level is known and then reschedule the examination. The inconvenience of such a protocol could be the impetus for freestanding imaging centers to develop good relationships with testing facilities that can supply creatinine results quickly. If a patient has known underlying renal disease, it might be a reason to consult a nephrologist. However, it is not necessary to consult a nephrologist prior to contrast administration for every patient with an elevated creatinine level. A consultation with a nephrologist would be an infrequent occurrence.

Preventive Measures

Though no current treatment can reverse or ameliorate CIN once it occurs, prevention is possible.6 If alternative imaging tests that do not use iodinated contrast cannot provide the necessary clinical information, preventive measures must be used. The damage associated with contrast agents can be minimized by using lower doses of contrast medium. Radiologists should, therefore, use the smallest volume of contrast needed to obtain images of clinical importance.

Hydration lowers the risk of renal failure and is especially important for patients who have mild renal insufficiency, diabetes, or multiple myeloma. Even for patients without such problems, hydration with saline solution is the primary intervention for preventing CIN. This method is based on the theory that hydration affects multiple risk factors, including decreasing the activity of the renin-angiotensin system, reducing the levels of other vasoconstrictive hormones, preventing tubular obstruction, and diluting the contrast medium in the tubule (which decreases any directly nephrotoxic effect of the contrast agent on the tubular epithelium).7

The following patients should receive hydration therapy using intravenous normal saline starting 2 to 4 hours before the administration of contrast: patients subject to repeated doses of contrast that are medically necessary within a 24 to 48 hour period; and patients whose creatinine is twice their normal range. A 1.4 creatinine may be normal for a large, muscular male but not a small nonmuscular female.

Hydration treatment should be continued during the radiographic procedure and should continue for 4 to 6 hours afterward. The duration of saline infusion should be extended starting sooner and ending later in the presence of more severe chronic kidney disease or underlying diabetic nephropathy.7

Another preventive method that may be considered is the infusion of sodium bicarbonate. This is a simple, safe, and inexpensive approach that is believed to work by alkalizing the tubular environment, thereby reducing the formation of free radicals and decreasing the incidence of acute renal failure occurring after exposure to contrast agents.8

An alternative to sodium bicarbonate is the administration of acetylcysteine solution. The mechanism of action is the trapping and destruction of free radicals. I personally prefer bicarbonate because I would rather prevent than trap the free radicals. The analogy would be the difference between putting up screens to keep out the flies or swatting them after they get into the house. But if you have to get rid of the flies, the administration of acetylcysteine has no downside.

In addition to measuring creatinine levels prior to employing a contrast medium, the physician, ideally the referring physician, should order the measurement of serum creatinine approximately 48 hours after contrast exposure to determine whether CIN has occurred. In most cases of CIN, serum creatinine begins to rise within 24 to 48 hours after contrast exposure, reaches a peak within 3 to 5 days, and then returns to baseline levels within 7 to 10 days. In more severe cases, the creatinine concentration may not peak until 5 to 10 days after contrast exposure, and the increase may be associated with oliguria.9

While hospital inpatients are at higher risk for CIN because they are typically more seriously ill than outpatients, radiologists have the advantage of having more control over inpatient care. It is possible to follow their creatinine levels and treat them quickly if there are problems, minimizing the effect of contrast. This reinforces how critically important it is for freestanding imaging facilities to develop good relationships with hospitals where they can send patients who experience contrast-related problems, and where they can send samples for laboratory testing to ascertain the risk of CIN.

Keys to Safer Scans

There are many situations in which contrast is useful but not essential, but contrast will always make an examination more accurate. It falls to radiologists to be aware of the ways that they can prevent or reduce the incidence of CIN in the patients coming through their facilities. You should always do everything you can to make the administration of contrast as safe as possible, which includes avoiding contrast known to have increased incidence of contrast-induced nephropathy.10 The risk of a patient developing CIN is very real. Radiologists must realize that by being well trained to manage this risk, they play vital roles in reducing the impact of CIN on their patients. n

George M. Ebert, MD, PhD, is vice chair and chief of section, CT, department of radiology, University of Vermont, Burlington.


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