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Published online before print March 16, 2006, 10.1148/radiol.2392050413
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(Radiology 2006;239:392-397.)
© RSNA, 2006

Contrast Media

Risk of Nephropathy after Intravenous Administration of Contrast Material: A Critical Literature Analysis1

Qasim Ali Rao, MD and Jeffrey H. Newhouse, MD

1 From the Department of Radiology, Columbia University Medical Center, Room 3-250, 177 Fort Washington Ave, New York, NY 10032. Received March 11, 2005; revision requested May 2; revision received June 16; final version accepted June 27. Address correspondence to J.H.N. (e-mail: jhn2{at}columbia.edu).


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ADVANCE IN KNOWLEDGE
 References
 
Purpose: To assess the risk of nephropathy after administration of contrast material by reviewing the published literature on intravenous contrast material administration and by separating reports with appropriate control measures from those without such measures.

Materials and Methods: The MEDLINE database was searched for articles published from October 1966 to September 2004 that contained the phrases "contrast," "contrast medium," "contrast media," or "radiocontrast" and any of the words or phrases "nephrotoxicity," "nephropathy," kidney failure," or "renal failure." The identified publications were reviewed and limited to original clinical series. Studies were categorized according to the route of contrast material administration. Those in which an identifiable group of patients received contrast material intravenously were further evaluated to determine which studies compared results with those from a control group of patients who did not receive contrast material.

Results: Only 40 (1.3%) of 3081 publications had patients who received contrast material intravenously. Of these, only two publications had control groups of patients who received no contrast material. The incidence of postcontrast nephropathy in these two series was not substantially different from that in the control groups.

Conclusion: Properly controlled clinical studies of intravenously administered radiographic contrast media fail to demonstrate renal damage.

© RSNA, 2006


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ADVANCE IN KNOWLEDGE
 References
 
The concept that intravascular administration of iodinated radiographic contrast media can cause renal dysfunction is nearly universally accepted. Contrast material has been associated with acute renal failure for nearly half a century (1) and is frequently cited as one of the most common causes of acute renal dysfunction in hospitalized patients (2–6). The risk is believed to be proportional to the severity of any level of preexisting renal failure—usually estimated with plasma creatinine levels—and to be increased in patients with long-standing diabetes. The American College of Radiology (7) has published guidelines for use of contrast media in patients with renal failure, and many radiology practices routinely require determination of serum creatinine levels in all patients before it is decided whether to administer contrast media (8).

Supporting the concept of contrast material–induced nephropathy are literally hundreds of publications on series of patients who have received contrast material, some of whom experience elevations in creatinine levels afterwards. Clinical experiments have assessed the effects of concurrent diseases such as preexisting renal failure, diabetes, hypertension, and multiple myeloma and have evaluated the effects of advanced age; contrast material dose, type, and route of administration; and a variety of treatments before or after contrast material administration (1). But despite the voluminous accounting of patients who have received contrast material and subsequently experienced degrees of renal failure, we believe that the absence of critical controls in nearly all of the published series and the extrapolation of data results from cardiac angiography to patients receiving intravenous contrast material may have led to an overestimation of the risk of intravenous contrast material administration to renal function.

Many of the published studies compare serial postcontrast creatinine measurements with each patient's precontrast creatinine level and ascribe any increase in creatinine level to the effects of contrast media (9–46). This constitutes a post hoc, ergo propter hoc fallacy: Increases in creatinine level after contrast material administration may have causes other than the contrast material itself, especially since many series involve hospitalized patients who are likely to have concurrent conditions that affect renal function (6,47). This possibility can only be assessed with a control group of similar patients who undergo serial creatinine measurements but do not receive contrast material. And patients who receive contrast material in the course of cardiac catheterization may undergo procedural complications that can affect renal perfusion, such as fluid restriction, arrhythmia, myocardial infarction, hypotension, hemorrhage, and other vascular complications (48), which do not occur to the same degree after intravenous contrast material injections.

We hypothesized that it is likely that published studies do not include appropriate control patients to confirm a serious risk to renal function of intravenous contrast material administration. Thus, we undertook our study to assess the risk of postcontrast nephropathy by reviewing the published literature on intravenous contrast material administration and by separating reports with appropriate control measures from those without such measures.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 ADVANCE IN KNOWLEDGE
 References
 
Initial Literature Searches
The MEDLINE database was searched (Q.A.R.) for articles published from October 1966 to September 1, 2004, looking for any of the words or phrases "contrast," "contrast medium," "contrast media," or "radiocontrast" and any of the words or phrases "nephrotoxicity," "nephropathy," "kidney failure," or "renal failure." The identified publications were limited to human studies.

To be certain that the list was complete, the MEDLINE database was again searched for the years 1993 to 2004 by using the same search terms as were used in the first MEDLINE search but limiting the articles to reviews. The complete bibliographies of all retrieved reviews were then inspected to determine whether they contained any articles not included in the two major searches; no such article was found.

Final Literature Included in Study
The list was then analyzed (Q.A.R.) and was limited to articles that described original clinical series; case reports, reviews, tutorials, letters, meta-analyses, guidelines for management, and literature reviews were excluded, as were articles addressing contrast media for sonography and magnetic resonance imaging and the use of gadolinium-based contrast media for computed tomography (CT). The list was then restricted by both authors in collaboration to series in which contrast material was always delivered intravenously and series in which contrast material was administered with more than one route but in which results in patients receiving contrast material intravenously could be distinguished from results in patients receiving contrast material via other routes. No limitations were imposed on the basis of the type of study performed; that is, series with patients receiving intravenous contrast material to undergo CT, excretory urography, and digital angiography were all included.

Analysis
Patients receiving intravenous contrast agents were divided into a group in which all described subjects received contrast material, with the precontrast serum creatinine levels used as each patient's control for determining whether postcontrast nephropathy occurred, and a group in which patients received contrast material were analyzed along with a control group of patients who did not receive contrast material to determine the incidence of contrast material–induced nephropathy. Criteria for identifying nephropathy were those proposed in each publication. Decisions regarding presence or absence of controls were made by each author independently; subsequent comparison of decisions revealed no disagreement.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 ADVANCE IN KNOWLEDGE
 References
 
The original MEDLINE search yielded 3081 publications, of which only 40 (9–46,49,50) were found that reported renal function in humans after intravenous contrast agent administration; 31 of these purported to demonstrate contrast material–induced nephropathy (one reported only excreted enzyme levels and did not assess serum creatinine levels), and nine claimed that contrast material did not affect renal function. In only two of the 40 articles (49,50) was the incidence of postcontrast renal dysfunction compared with the incidence of renal dysfunction in a matched control group of patients who did not receive contrast material.

In one publication (49), serum creatinine levels were determined before and for 2 days after contrast-enhanced brain CT (contrast medium volume, 60–350 mL; type not specified) in 193 patients and after nonenhanced brain CT in 233 control patients. Renal dysfunction following CT, defined as an increase in serum creatinine to a level higher than 106.1 µmol/L (1.2 mg/dL) and at least 50% higher than baseline, developed in four (2.1%) patients who had infusion of contrast material and in three (1.3%) patients who had no infusion; the difference was not significant. In a high-risk subgroup (serum creatinine level at least 132.6 µmol/L [1.5 mg/dL] or diabetes mellitus), renal failure developed in none of the 19 patients who received contrast material and in two (4.3%) of 46 patients who did not receive contrast material. It was concluded that authors of previous uncontrolled studies may have overestimated the risk of renal failure induced by contrast material.

In the other publication (50), the hypothesis that there is no difference in the change in serum creatinine level following CT among patients given high-osmolality contrast material, low-osmolality contrast material, or no contrast material was tested. In 292 inpatients high-osmolality contrast material was used, in 187 low-osmolality contrast material was used, and in 405 no contrast material was used. Renal impairment was defined as a maximal increase in the serum creatinine level of 50% or more or greater than 0.44 mmol/L (0.5 mg/dL) from the baseline level on at least one of the subsequent 4 days. Renal impairment was seen in 4% (12 of 292), 12% (23 of 187), and 4% (16 of 405) of patients given high-osmolality contrast material, low-osmolality contrast material, or no contrast material, respectively. The 51 patients who developed renal impairment were matched with 150 case controls for age, sex, type of contrast agent, and preexisting renal impairment. Without further analysis it might seem that the high-osmolality contrast material did not increase the likelihood of renal dysfunction but that low-osmolality contrast material did, in contradistinction to findings of other studies (27,37), which showed that low-osmolality contrast material was less likely to be followed by renal dysfunction than high-osmolality contrast material. Further analysis, however, suggested otherwise.

First, among all patients who received contrast material, low-osmolality contrast material was chosen for each patient who had renal or cardiac impairment, dehydration, diabetes, myelomatosis, or sickle-cell disease; clearly, this was a group with greater risk factors for acute renal dysfunction than the other two groups. Also, among this group, in-hospital mortality was 12.3%; mortality was 4.1% and 6.2% in the high-osmolality contrast material group and the no contrast material group, respectively, and the case-control group demonstrated risk factors that substantially increased the risk of renal dysfunction as well. The authors concluded that the apparent risk associated with low-osmolality contrast material was most likely due to differences in risk factors other than contrast material use and type.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
ADVANCE IN KNOWLEDGE
 References
 
Contrast agents have been implicated as one of the most common causes of acute renal dysfunction. The literature addressing the incidence of contrast-induced nephropathy is voluminous, as attested by the thousands of articles our searches revealed. Nearly all support the view that contrast material causes renal dysfunction.

To our knowledge, the earliest publications about patients who had acute renal failure after receiving contrast material were case reports; virtually all patients had multiple myeloma (51–56). Subsequently, reports of larger numbers of patients appeared (10,12,18,20,25,26,29,44). None was a prospective series; in all, clinical records were searched for patients who had received contrast material and who had renal dysfunction shortly afterward. Without knowledge of the numbers of patients from whom the reported groups were drawn, the risk of renal dysfunction following contrast material administration could not be estimated. Then, retrospective (34,36,46) and prospective (19,30–33,40,43) studies appeared in which the proportion of studied patients who experienced postcontrast renal dysfunction could be estimated. The results differed; some found that a significant fraction of patients with chronic renal failure experienced postcontrast renal dysfunction, especially if diabetes was present. None had parallel control arms of patients not receiving contrast material.

Several publications also appeared in which renal function was compared after intravenous administration of two different contrast agents (15,17,22,27,31,32,39). Conflicting conclusions were reached, but within the discussions of all articles, the assumption that some degree of contrast agent nephrotoxicity existed was clear. None had controls with patients who did not receive contrast material.

Finally, series have been published in which the authors purported to assess the effect of two prophylactic regimens (11,42) on postcontrast renal dysfunction in patients with chronic renal insufficiency. In one series (11), 250 mL of 20% mannitol was administered to subjects 1 hour before the contrast material. In the other series (42), 600 mg of acetylcysteine was administered orally twice on the day before contrast agent administration and twice on the same day as contrast agent administration. Both the experimental group and the control group received 1 (mL/kg)/hr of saline for 12 hours before and 12 hours after contrast agent administration. Neither study had a control group of patients who did not receive contrast material. Both regimens diminished the incidence of renal dysfunction, but these results could simply mean that transient elevations of creatinine levels in any patients with chronic renal failure—with or without contrast agent administration—are less likely to occur in the few days following each treatment.

Notwithstanding the numbers of these articles, scientifically rigorous support of the possibility that renal dysfunction after contrast agent administration is in fact caused by the contrast agent can only be supplied by studies in which the incidence of renal dysfunction in a control group of patients who do not receive contrast material is compared with that in patients who do receive contrast material. We could only find two trials that were performed with such parallel control groups in whom the fluctuations in serum creatinine values were studied simultaneously with a group receiving intravenous contrast material for the same period of time (49,50). Both of these articles clearly state that there is no significant difference in the incidence of contrast material–induced nephropathy after intravenous procedures, which suggests to us that the incidence of contrast-induced nephropathy after intravenous procedures has been exaggerated to an unknown degree.

Inflated estimates of the danger of postcontrast nephropathy may also have originated from studies in patients who have undergone cardiac catheterization. Cardiac catheterization may impose or cause a number of conditions that may result in transient hypotension and/or renal ischemia (48). Patients may undergo fluid restriction prior to the procedure. During the procedure, they may experience arrhythmias, periods of diminished cardiac output, hypotension, and even frank myocardial infarction. They may have strokes and, given that some of the strokes are undoubtedly embolic, as some of the myocardial infarctions can be presumed to be, and given that many have aortic plaques, which may be dislodged during the procedure, it would be unlikely that the kidneys could always escape embolization. Also, hematomas after catheterization may form in the retroperitoneum and lower extremity, which, when large, may also produce renal hypoperfusion. These all have the potential to diminish renal perfusion and produce an increase in serum creatinine levels, which may erroneously be ascribed to the contrast agent itself.

There is one publication (35) in which the incidence of renal dysfunction after cardiac angiography was compared with that found after intravenous contrast-enhanced CT; cardiac angiography was followed by a significantly higher likelihood of renal dysfunction. Authors of another study (27) compared the rates of postcontrast nephropathy in their own patients with those found after cardiac angiography in two series from earlier literature (57,58) and reported a higher incidence of renal dysfunction after cardiac angiography.

Authors of two other studies (15,31) compared renal dysfunction after intravenous contrast-enhanced CT with that found after aortography and peripheral angiography; no difference in risk was demonstrated. These findings lend support to the concept that factors associated with cardiac angiography but not with peripheral contrast agent administration may be those responsible for renal dysfunction.

Many studies of postcontrast renal dysfunction are performed in inpatients (9,31,35,49,50). To study outpatients who would be required to return to the hospital or clinic for several blood samples is not always feasible. Patients sufficiently ill that they must remain in the hospital for 4 or more consecutive days are likely to have diseases, such as atherosclerosis, hypertension, or diabetes, or to receive treatments that potentially diminish renal function, such as shock, surgery, and nephrotoxic drugs. Hospitalized patients with these conditions are likely to have increases in serum creatinine levels that have nothing to do with contrast agent administration and that, in the absence of appropriate control groups, may be incorrectly ascribed to contrast agent administration.

Yet another factor that may cause renal dysfunction to be incorrectly ascribed to contrast material is the patient's preprocedure preparation. In one study (43), the preparatory regimen (12 hours of fluid restriction, palmitic acid as a laxative, and an enema) was followed by a significant increase in creatinine level above the baseline value in 10 of 124 patients before the contrast agent was administered; this group constituted 37% of all the patients whose creatinine level increased.

Notwithstanding the arguments that the risk of postcontrast nephropathy may have been overestimated in the past, we do not claim that intravenous contrast material never reduces renal function. Authors of the two aforementioned articles in which patient groups who received contrast material were compared with control groups who did not receive contrast material and who found no significant difference in the incidence of increase in creatinine level (49,50) may have failed to recognize contrast agent nephrotoxicity that really took place. In neither series were the patients randomly assigned to their groups; in each case, patients with greater risk factors for renal function deterioration may have been preferentially steered to the control groups, which masked the real nephrotoxic effects of contrast material. In both experiments, a threshold of a 50% increase in serum creatinine level was established to define acute renal dysfunction. If a threshold of a 25% or 33% increase had been used, as in some other investigations, different rates of postcontrast nephropathy might have been encountered. Finally, the number of patients with diabetes and elevated precontrast creatinine levels may not have been sufficient to enable detection of a very small contrast agent nephrotoxicity risk.

There were several important limitations in our investigation. We were unable to assess the real risk to renal function with intravenous contrast agent administration; the absence of controls in most of the articles we reviewed and the absence of strict randomization in the two investigations that included controls prevent such an estimate. Although our findings revealed the necessity for further investigation, they are insufficient to support recommending a change in current clinical practice.

From this critical review, we conclude that controlled series that support the hypothesis that intravenously administered contrast material is potentially nephrotoxic are conspicuously absent and that both this lack of control data and a tendency not to distinguish series involving intravenous contrast material from those involving cardiac angiography with its attendant risks are possibly responsible for a consensus about the erroneously exaggerated risk of renal dysfunction due to intravenous contrast material. Only a large clinical study with appropriate control groups, matched for concurrent risks of renal dysfunction and with random group assignment of patients, will be able to assess the risk accurately.


   ADVANCE IN KNOWLEDGE
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ADVANCE IN KNOWLEDGE
References
 


   FOOTNOTES
 
Author contributions: Guarantors of integrity of entire study, Q.A.R., J.H.N.; study concepts/study design or data acquisition or data analysis/interpretation, Q.A.R., J.H.N.; manuscript drafting or manuscript revision for important intellectual content, Q.A.R., J.H.N.; manuscript final version approval, Q.A.R., J.H.N.; literature research, Q.A.R., J.H.N.; and manuscript editing, Q.A.R., J.H.N.

Authors stated no financial relationship to disclose.


   References
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ADVANCE IN KNOWLEDGE
 References
 

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J. H. Ellis and R. H. Cohan
Reducing the Risk of Contrast-Induced Nephropathy: A Perspective on the Controversies
Am. J. Roentgenol., June 1, 2009; 192(6): 1544 - 1549.
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R. J. Bruce, A. Djamali, K. Shinki, S. J. Michel, J. P. Fine, and M. A. Pozniak
Background Fluctuation of Kidney Function Versus Contrast-Induced Nephrotoxicity
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E. Ledneva, S. Karie, V. Launay-Vacher, N. Janus, and G. Deray
Renal Safety of Gadolinium-based Contrast Media in Patients with Chronic Renal Insufficiency
Radiology, March 1, 2009; 250(3): 618 - 628.
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C. Pering, P. Lengsfeld, P. Seidensticker, U. J. Schoepf, and P. Costello
Iso- versus Low-Osmolar Contrast Media and Contrast Medium-induced Nephropathy
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Which Study When? Is Gadolinium-enhanced MR Imaging Safer than Iodine-enhanced CT?
Radiology, October 1, 2008; 249(1): 3 - 8.
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Which Study When? Iodinated Contrast-enhanced CT Versus Gadolinium-enhanced MR Imaging
Radiology, October 1, 2008; 249(1): 9 - 15.
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S. Langner, S. Stumpe, M. Kirsch, M. Petrik, and N. Hosten
No Increased Risk for Contrast-Induced Nephropathy after Multiple CT Perfusion Studies of the Brain with a Nonionic, Dimeric, Iso-Osmolal Contrast Medium
AJNR Am. J. Neuroradiol., September 1, 2008; 29(8): 1525 - 1529.
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J. H. Newhouse, D. Kho, Q. A. Rao, and J. Starren
Frequency of Serum Creatinine Changes in the Absence of Iodinated Contrast Material: Implications for Studies of Contrast Nephrotoxicity
Am. J. Roentgenol., August 1, 2008; 191(2): 376 - 382.
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D. A. Baumgarten and J. H. Ellis
Contrast-Induced Nephropathy: Contrast Material Not Required?
Am. J. Roentgenol., August 1, 2008; 191(2): 383 - 386.
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M. J. Kuhn, N. Chen, D. V. Sahani, D. Reimer, E. J. R. van Beek, J. P. Heiken, and G. J. So
The PREDICT Study: A Randomized Double-Blind Comparison of Contrast-Induced Nephropathy After Low- or Isoosmolar Contrast Agent Exposure
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B. R. Herts, E. Schneider, E. D. Poggio, N. A. Obuchowski, and M. E. Baker
Identifying Outpatients with Renal Insufficiency before Contrast-enhanced CT by Using Estimated Glomerular Filtration Rates versus Serum Creatinine Levels
Radiology, July 1, 2008; 248(1): 106 - 113.
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M J Fernandez Cabezudo, G Petroianu, B Al-Ramadi, and R D Langer
Iosimenol, a new non-ionic dimeric contrast medium, does not induce immunoreactivity in the popliteal lymph node assay
Br. J. Radiol., September 1, 2007; 80(957): 713 - 718.
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A. L. Krol, I. Dzialowski, J. Roy, V. Puetz, S. Subramaniam, S. B. Coutts, and A. M. Demchuk
Incidence of Radiocontrast Nephropathy in Patients Undergoing Acute Stroke Computed Tomography Angiography
Stroke, August 1, 2007; 38(8): 2364 - 2366.
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R. W. Katzberg and B. J. Barrett
Risk of Iodinated Contrast Material-induced Nephropathy with Intravenous Administration
Radiology, June 1, 2007; 243(3): 622 - 628.
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B. Murphy, Q. A. Rao, and J. H. Newhouse
Contrast Material-induced Nephropathy
Radiology, May 1, 2007; 243(2): 606 - 606.
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