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DOI:10.2214/AJR.07.3280
AJR 2008; 191:376-382
© American Roentgen Ray Society

Original Research

Frequency of Serum Creatinine Changes in the Absence of Iodinated Contrast Material: Implications for Studies of Contrast Nephrotoxicity

Jeffrey H. Newhouse1, David Kho1,2, Qasim A. Rao1,3 and Justin Starren1,4,5

1 Department of Radiology, Columbia University Medical Center, 630 W 168th St., New York, NY 10032.
2 Present address: Department of Radiology, Winthrop University Hospital, Mineola, NY.
3 Present address: Department of Radiology, Bridgeport Hospital, Bridgeport, CT.
4 Department of Medical Informatics, Columbia University Medical Center, New York, NY.
5 Present address: Biomedical Informatics Research Center, Marshfield Clinic Research Foundation, Marshfield, WI.

Received October 9, 2007; accepted after revision February 12, 2008.

 
Address correspondence to J. H. Newhouse (jhn2{at}columbia.edu).

CME

This article is available for CME credit. See www.arrs.org for more information.


Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
OBJECTIVE. Most studies of contrast-induced nephropathy lack controls to distinguish it from nephropathy from other causes. We assessed the frequency and magnitude of serum creatinine changes in patients not receiving iodinated contrast material to compare with creatinine changes in publications regarding contrast nephropathy.

MATERIALS AND METHODS. From the electronic medical records of an academic medical center, adults with creatinine determinations on five consecutive days who had not received contrast material during the previous 10 days were identified. The first creatinine level was compared with those on subsequent days. We calculated the frequency with which these levels exceeded thresholds used to identify contrast nephropathy in previous publications.

RESULTS. Among 32,161 patients, more than half showed a change of at least 25% and more than two fifths, a change of at least 0.4 mg/dL. Among patients with baseline creatinine levels of 0.6–1.2 mg/dL, increases of at least 25%, 33%, and 50% occurred in 27%, 19%, and 11% of patients, respectively. Increases of 0.4, 0.6, and 1.0 mg/dL occurred in 13%, 7%, and 3% of patients. Among patients with baseline creatinine levels greater than 2.0 mg/dL, increases of at least 25%, 33%, and 50% occurred in 16%, 12%, and 7%. Increases of 0.4, 0.6, and 1.0 mg/dL occurred in 33%, 26%, and 18%. These increases were not different from the incidences of contrast nephropathy previously published.

CONCLUSION. The creatinine level increases in patients who are not receiving contrast material as often as it does in published series of patients who are receiving contrast material. The role of contrast material in nephropathy may have been overestimated.

Keywords: contrast material • iodinated contrast material • nephropathy • nephrotoxicity • renal failure


Introduction
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 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Iodinated radiographic contrast agents have been thought for decades to be responsible for subsequent renal dysfunction [1–5]. A widely quoted article states that contrast material is the third most common cause of renal failure among hospitalized patients [6]. The concept of contrast-induced nephropathy is supported by many articles describing patients who have received contrast material and subsequently experienced creatinine increases. To minimize the risk, the American College of Radiology and the European Society of Uroradiology have developed guidelines for administering contrast media in patients with renal failure. A serum creatinine determination has become a prerequisite for contrast-enhanced studies in many radiology practices [7].

Yet some difference of opinion exists regarding the nephrotoxic potential of contrast material when administered IV. The risk of IV contrast material may have been exaggerated in the literature, and nearly all of the clinical series designed to assess the risk of contrast material have been performed without control groups of patients who did not receive contrast material [8]. Only two series have compared the incidence of renal dysfunction after administration of IV contrast material (postcontrast) with the incidence of renal dysfunction in control subjects not receiving contrast material, and neither found any statistically significant difference in renal function between the two groups [9, 10]. Also, the incidence of nephropathy after angiocardiography [11–13] has been assumed to apply to patients who receive contrast material IV; however, patients who have contrast material in the course of cardiac catheterization may undergo procedural complications that can affect renal perfusion, such as fluid restriction, arrhythmias, myocardial infarction, hypotension, hemorrhage, and other vascular complications [14] that do not occur to the same degree after IV contrast injections.

The published criteria by which to identify cases of contrast-induced nephropathy are not uniform. Most investigators have used serum creatinine determinations to assess renal function after IV contrast material has been given; a few have calculated creatinine clearance [15] and a few have measured enzymuria [16–18]. A variety of thresholds of elevations in creatinine levels have been used to identify patients thought to have contrast-induced nephropathy; increases of 20% [19], 25% [20–24], 33% [11], and 50% [9] over the precontrast creatinine levels have been used, as have absolute increases of 0.2 [25], 0.4 [11], 0.5 [26], and 1.0 [27] mg/dL. The time between the initial creatinine determination and the administration of contrast material has varied from as little as an hour to as much as 2 weeks, the number of creatinine determinations has ranged from one to five, and the time after contrast administration that these creatinine levels have been measured has ranged from an hour to 2 weeks.

Without concurrent control groups in most of these series, it is difficult to estimate the probability that the reported creatinine elevations after the administration of contrast material were, in fact, caused by contrast material. To determine whether creatinine variations caused by the combination of all conditions other than contrast administration might be frequent enough to have been responsible for an important fraction of the cases of presumed contrast nephrotoxicity, we assessed the variability in creatinine levels in clinical data extracted from 10 years of records in the clinical data warehouse of an urban academic medical center. We compared the incidence of creatinine increases in a non-contrast-exposed population with those reported in previously published series of contrast-exposed patients.

Because the term "contrast-induced nephropathy" presumes causality that may not exist, in this article we will use the term "postcontrast creatinine increase."


Materials and Methods
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 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Patients
This study was approved by the relevant institutional review board and the HIPAA privacy committee, and informed consent was waived for this retrospective study. We searched the medical records of the clinical data warehouse of a major medical center. This warehouse is a relational, longitudinal repository that contains electronic records of more than 2 million patients dating from 1989 [28, 29]. Electronic records for laboratory, radiology, and cardiology have been stored in coded form since the mid 1990s.

Database Search
The clinical data warehouse was searched for the period from January 1, 1995, through December 8, 2004. All patients with serum or plasma creatinine measurements on five consecutive days were identified. For each day in which more than one creatinine measurement was made, the first creatinine value of the day was selected for later analysis. For each of these patients, records of all radiology and cardiology examinations were retrieved for the period beginning 10 days before the first creatinine measurement and ending on the day of the last creatinine measurement.

The clinical data warehouse was searched for all radiology and cardiology procedure codes during the period of interest. In total, 562 radiology procedure codes and 30 cardiology procedural codes were used to identify studies. These studies were manually classified into those involving no contrast material and those involving any type of contrast material (parenteral and oral; iodinated, noniodinated, and radioactive). Only patients who had had studies involving no contrast material, or who had had no radiology or cardiology studies at all, were included in subsequent analyses. These findings were then used to classify all radiology and cardiology procedures during the period of interest for each patient.

Data Analysis
Data from the clinical data warehouse search were transferred to a MySQL (MySQL AB) database for further analysis. For each patient, only the first 5-day series of creatinine measurements was selected for analysis; subsequent series were excluded. The day of the baseline creatinine measurement was defined as day 0. Groups were stratified on the basis of baseline creatinine values. For subsequent days, both relative percentage and absolute changes from day 0 were computed.

Literature Comparison
We reviewed publications that reported series of patients who received IV contrast material and were evaluated for a postcontrast creatinine increase; the search was conducted through MEDLINE using topic search terms including "contrast material" and a variety of words and phrases denoting nephrotoxicity and renal failure or dysfunction. The list was narrowed by including only articles that reported renal function in terms of serum creatinine determinations (i.e., excluding those that reported only creatinine clearance or enzymuria), specified the threshold of postcontrast creatinine elevation used to diagnose nephropathy, and reported the interval between the precontrast creatinine level and contrast administration and the interval between contrast administration and the postcontrast creatinine determination. Articles that described the use of intracardiac or intraarterial contrast administration, or in which the route was not specified, were not analyzed.


Results
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 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
A total of 32,161 patients with serial creatinine levels recorded on five consecutive days and no prior contrast material administration were identified. The average baseline creatinine level on day 0 was 1.65 mg/dL (± 2.21 [SD] mg/dL). Average creatinine levels trended down slightly. The average on day 4 was 1.45 (± 1.78) mg/dL. Figure 1 summarizes the overall changes in creatinine levels. Both increases and decreases in creatinine occurred. The longer the interval after day 0, the greater the fraction of patients who exceeded each threshold for an increase or decrease. Cumulative frequencies (threshold changes that occurred on any of the days of the interval but that may have resolved by the end of the interval) are higher (Fig. 2). In other words, if a patient had a creatinine level of 1.0 mg/dL on day 0, 1.3 mg/dL on day 2, and 1.2 mg/dL on day 4, that patient would be included in the day-4 cumulative total (Fig. 2) but would be excluded from the day-4 noncumulative values (Fig. 1). For obvious reasons, the cumulative determination figure is more sensitive than a single spot measurement. Similar patterns are seen for absolute change in creatinine level (Fig. 3).


Figure 1
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  		Fig. 1 —Fraction of patients with threshold creatinine change. Figure shows fraction of patients having relative change in creatinine level at indicated percentage on a specific day versus day 0. Lower thresholds are more likely to be reached, and decreases are more common than increases. Totals sum to greater than 100% because higher percentage of change (e.g., 50%) is included in results for lower thresholds (e.g., 25%).

 

Figure 2
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  		Fig. 2 —Cumulative fraction of patients with fractional threshold creatinine change. Figure shows fraction of patients having a threshold change on any day up to indicated day versus day 0. Lower thresholds are more likely to be reached, and decreases are more common than increases. Totals sum to greater than 100% because higher percentage of change (e.g., 50%) is included in results for lower thresholds (e.g., 25%).

 

Figure 3
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  		Fig. 3 —Cumulative fraction of patients with absolute threshold creatinine change. Figure shows fraction of patients having a change of at least value indicated on any of the days up to indicated day versus day 0. Lower thresholds are more likely to be reached, and decreases are more common than increases. Totals sum to greater than 100% because higher thresholds (e.g., 1.0) are included in totals with lower thresholds.

 

The influence of baseline creatinine level on subsequent creatinine change was investigated. Significant fractions of patients in both the normal and the elevated creatinine populations showed creatinine changes above threshold. Table 1 summarizes the effect of initial creatinine for various thresholds expressed as percentage of change as well as in absolute creatinine change. As expected, higher initial creatinine values are associated with a lower frequency of a given percentage of change but a higher frequency of a given absolute change.


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  		TABLE 1: Effect of Initial Creatinine Level on Frequency of Change at Various Thresholds

 

Review of the literature revealed 19 articles [9–11, 20–25, 27, 30–38] that met all of the selection criteria. Criteria to identify postcontrast creatinine increase and rates of postcontrast creatinine increase varied widely among those articles. Rates of postcontrast creatinine increase ranged from 0% to 76% (the latter among patients with both chronic renal failure and long-standing diabetes); most were less than 20%. Figures 4A and 4B provides a graphic comparison of the observed frequencies of creatinine increase in our non-contrast-exposed population with previously reported incidences of postcontrast creatinine increase. The incidences from our data are higher than many reported in the contrast-exposed populations.


Figure 4
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  		Fig. 4A —Comparison of reported contrast-induced creatinine increase and observed frequencies. Frequencies observed in this study (percentage of increase [A] and absolute increase [B]) in our non-contrast-exposed population are indicated by solid circles. Open circles represent previously published data (also summarized in Table 2). Number adjacent to each open circle is number of corresponding publication in reference list. Overall risk of nephropathy in patients receiving contrast material is not clearly different from risk in patients who have not received it.

 

Figure 5
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  		Fig. 4B —Comparison of reported contrast-induced creatinine increase and observed frequencies. Frequencies observed in this study (percentage of increase [A] and absolute increase [B]) in our non-contrast-exposed population are indicated by solid circles. Open circles represent previously published data (also summarized in Table 2). Number adjacent to each open circle is number of corresponding publication in reference list. Overall risk of nephropathy in patients receiving contrast material is not clearly different from risk in patients who have not received it.

 

Discussion
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 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
This study shows that the frequency of significant creatinine change in the absence of contrast agents may be much higher than is commonly assumed. During the 5-day period, more than half the patients showed a change (up or down) of at least 25% and more than two fifths showed a change of at least 0.4 mg/dL. These changes occurred in patients with both normal and abnormal initial creatinine values and were undoubtedly caused by the entire range of conditions, treatments, and laboratory variations that may alter creatinine levels. Previous data using creatinine change as a de facto standard for contrast-induced nephropathy must be reevaluated in light of these results. Such attribution constitutes a post hoc, ergo propter hoc (after this, therefore because of this) logical fallacy [8].


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  		TABLE 2: Previously Published Articles Assessing Creatinine Increases After Contrast Administration

 

Multiple studies have compared a precontrast creatinine value with a postcontrast value and attributed any increase to the effect of contrast material [9, 15, 16, 19–26, 29–59] (Table 2). The incidence of significant creatinine increase in our patients who did not receive iodinated contrast material is comparable to previously reported incidences of creatinine change after contrast material was administered. It is clear that all postimaging creatinine changes cannot be ascribed to the effect of contrast agents, and that the interpretation of uncontrolled studies is fraught with significant risk. A variety of other factors might have affected the patients' renal function in the published studies. Many studies involved hospitalized patients who were particularly likely to have concurrent conditions that affect renal function [6, 60].

In the absence of concurrent randomized controls, such studies can only be evaluated against a control group of patients under similar conditions who did not receive contrast material. The results of our study approximate such a control. We do not claim that our population of patients is identical to those who received contrast material and were described in the earlier publications; nevertheless, it is likely that they are similar. Our patients included those with other risk factors for short-term creatinine changes; patients who were receiving drugs and other nephrotoxic agents and who had acute glomerulonephritis, hemolysis, rhabdomyolysis, shock and reduced cardiac output, acute renal vascular occlusion, surgery, burns, sepsis, hepatorenal syndrome, and obstruction were not excluded from our study. In the previous articles, the results of which are summarized in Figures 4A and 4B, the studied groups also did not have these conditions excluded [9–11, 20–25, 27, 30–38]. Only three studies [25, 27, 33] investigated populations clearly different from ours in that all of the studied patients had diabetes.

The results of this study are consistent with the limited literature on prospective, randomized studies involving IV contrast material. The review by Rao and Newhouse [8] identified only two trials that were performed with prospective parallel control groups in which the fluctuations in serum creatinine values were studied simultaneously with the group receiving the IV contrast agent for the same period of time [9, 10]. Both of those articles clearly state that there is no statistically significant increase in the incidence of postcontrast creatinine increase after IV procedures as compared with a contrast material–free control group.

We have compared our data only with prior articles that describe patients who have received contrast material IV. Most of the articles in the literature dealing with postcontrast creatinine increase describe patients who have undergone cardiac angiography. Cardiac catheterization may impose or cause a number of conditions that may cause transient hypotension or renal ischemia [14]. Patients may undergo fluid restriction before the procedure. During the procedure they may experience arrhythmias, periods of diminished cardiac output, hypotension, and even frank myocardial infarction. Patients undergoing cardiac catheterization are at increased risk for aortic plaques, which may be dislodged during the procedure, leading to possible embolic insults to the kidneys. Occasionally, large postcatheterization hematomas may develop in the retroperitoneum or lower extremity, potentially causing hypovolemia and affecting renal perfusion. Thus, a variety of events sometimes associated with cardiac catheterization may diminish renal perfusion and lead to an increase in the serum creatinine levels that may be erroneously ascribed to the contrast agent itself. Consistent with this are studies that find a significantly higher incidence of renal dysfunction after catheter angiocardiography than after CT with IV contrast material [11–13, 23]. Therefore, we caution that the results of experiments with patients who have had cardiac angiography should not be assumed to apply to patients who undergo IV contrast administration.

In addition to factors related to the procedure itself, the preparation of the patient before any imaging study may affect later creatinine levels. In one study, a preparatory regimen (12 hours of fluid restriction, palmitic acid as a laxative, and an enema) was followed by a significant rise in creatinine above the baseline value in 8% (10/124) of patients before the contrast material was even administered [32].

Another concern with the design of many prior studies is that they were one-sided—only creatinine increases were evaluated. Our study shows that the frequency of creatinine decreases is comparable to that of increases. Because only creatinine increases were examined in the previously published series, the incidence of significant creatinine decreases after contrast material administration is unknown. A hypothetic investigation that assessed only the frequency with which creatinine levels decreased to levels below a certain threshold would (absent appropriate controls) conclude that IV iodinated contrast agents might even be nephroprotective, as other osmotic diuretic agents may be [22].

Our study also shows that the higher the initial creatinine level, the more likely that any given creatinine increase threshold will be exceeded. Contrast nephropathy has long been held to be a greater risk in patients with initially elevated creatinine levels; if this conclusion turns out to have been due to lack of control groups, the tendency for higher creatinine levels to exhibit greater variations may have been responsible for the error.

Our study has a number of limitations. Our patients constitute a group who had serial creatinine levels measured for several days; it could be argued that they are a group at greater risk for renal dysfunction than patients whose physicians did not find reasons to order frequent serum creatinine measurements. The average renal function of our overall group improved over the four analyzed days, however, which is not consistent with their being at particularly high risk. Also, most of the patients from whom our data are drawn were hospitalized years later than the patients in the published series; because there has been a recent tendency to hospitalize only relatively sick patients, our subjects may have had more severe illnesses than those in earlier studies. Because our study uses routine clinical laboratory results rather than reference laboratory results, it is certain that some of the more than 160,000 creatinine values analyzed are erroneous—but this limitation is shared by many of the prior studies. Because the records searched are limited to a single institution, it is possible that some patients received a contrast-enhanced study at another institution within the 10 days before the observed creatinine levels were measured. However, given the medical center's role as the primary supplier of both primary and secondary care for its patient population, most contrast imaging studies performed on medical center patients are performed at the medical center, including preadmission studies.

We conclude that because serum creatinine levels change frequently in the absence of iodinated contrast material, prior studies of the relationship between iodinated contrast material and renal function must be interpreted with caution, and that future experiments should have appropriate controls. We do not claim that IV contrast material never induces nephropathy, but it may do so less frequently and severely than previously thought. If subsequent experimentation proves its safety, it could be used more frequently in patients with renal failure, which could both increase the diagnostic capacity of CT and avoid the cost and risk of gadolinium-enhanced MRI.


References
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 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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