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Genitourinary Imaging |
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Barbara Jeschke, MD,
Leopoldo Lutilsky, MD,
Wolfgang Weiss, MD,
Hermann Salmhofer, MD and
Meinhard Classen, MD
1 From the II. Medizinische Klinik, Klinische Chemie (W.H., K.I., M.P., U.S., B.J., H.S., M.C.); Institut für Medizinische Statistik und Epidemiologie (M.H.), I. Medizinische Klinik (L.L.), and Department of Radiology (W.W.), Klinikum Rechts der Isar, Technical University of Munich, Ismaningerstrasse 22, Station 2/11, D-81675 Munich, Germany. Received March 17, 2001; revision requested April 30; final revision received November 7; accepted December 6. Address correspondence to W.H. (e-mail: wolfgg.huber@t-online.de).
2 Dr Schweigart died in April 2000.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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MATERIALS AND METHODS: One hundred patients with serum creatinine levels of 1.3 mg/dL (114.3 µmol/L) or greater were randomly assigned to intravenously receive 200 mg theophylline or saline 30 minutes before administration of 100 mL or more of low-osmolarity contrast medium arterially (72 [72%] patients) or intravenously (28 [28%] patients).
RESULTS: Patients receiving theophylline and control subjects were comparable with regard to risk factors for contrast-induced nephropathy such as mean serum creatinine level before contrast medium administration (2.07 mg/dL ± 0.94 [SD] [182.9 µmol/L ± 83.1] vs 1.92 mg/dL ± 0.76 [169.7 µmol/L ± 67.2], respectively), amount of contrast medium (196.5 mL ± 84.1 vs 216.6 mL ± 95.0, respectively), and diabetes prevalence. Theophylline prophylaxis significantly reduced the incidence of contrast material–induced nephropathy (4% vs 16%; P = .046). With theophylline, the mean serum creatinine level decreased nonsignificantly 12 (1.98 mg/dL ± 0.77 [175.0 µmol/L ± 68.1]; P = .09), 24 (1.97 mg/dL ± 0.75 [174.1 µmol/L ± 68.1]; P = .99), and 48 (1.94 mg/dL ± 0.77 [171.5 µmol/L ± 68.1]; P = .99)(1.94 mg/dL ± 0.77 [171.5 µmol/L ± 68.1]; P = .99) hours after contrast medium administration. With a placebo, serum creatinine level significantly increased 24 hours after contrast medium administration (2.01 mg/dL ± 0.89 [177.7 µmol/L ± 78.7]; P = .006). Urinary N-acetyl-ß-glucosaminidase level did not change with theophylline administration but significantly (P = .034) increased 24 hours after contrast medium administration with the placebo.
CONCLUSION: Prophylactic administration of 200 mg theophylline reduces the incidence of contrast material–induced nephropathy in patients with chronic renal insufficiency.
© RSNA, 2002
Index terms: Angiography, complications, 81.1242, 81.44 • Contrast media, complications, 81.44 • Contrast media, effects, 81.44 • Coronary angiography, complications, 81.44 • Kidney, failure, 81.44 • Theophylline
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The frequency of contrast material–induced nephropathy strongly depends on a number of risk factors and in the worst cases is more than 50% (5). The most important risk factors (6–10) are renal insufficiency (serum creatinine level 
1.3 mg/dL [114.4 µmol/L), diabetes, and high doses of contrast medium (critical threshold between 125 [7] and 200 mL [10]). Further risk factors are dehydration, nephrotoxic medication such as acetylsalicylic acid, intraarterial administration of contrast medium, and age less than 70 years (10).
Due to the clinical relevance of contrast material–induced nephropathy, a large number of prophylactic procedures have been investigated. Until recently, randomized studies (11,12) had shown a substantial reduction of contrast material–induced nephropathy, according to Barrett and Parfrey’s (2) definition, only with the use of low- instead of high-osmolarity contrast medium. Recently, in another controlled study (13), a prophylactic effect of the antioxidant acetylcysteine was demonstrated after intravenous administration of small amounts of contrast medium. The beneficial effect of an antioxidant suggests that oxygen free radicals play an important role in the pathogenesis of contrast-induced nephropathy.
Adenosine, another key mediator of contrast material–induced nephropathy, pathophysiologically functions even further upstream than do oxygen radicals (14–16), which explains the results of several clinical studies (17–20) in which the competitive adenosine antagonist theophylline was used as prophylaxis. However, these studies either involved relatively small numbers of patients or showed a benefit detectable only with very sensitive methods. Unfortunately, the investigators in these studies excluded patients with severely impaired renal function and common risk factors, such as taking acetylsalicylic acid (17) or having heart failure (18), or did not set a lower limit for the amount of contrast medium administered (20). Thus, the high-risk patients who might have profited most from theophylline prophylaxis were excluded.
Therefore, the purpose of our prospective study was to investigate whether the adenosine antagonist theophylline reduces the incidence of contrast material–induced nephropathy in high-risk patients who have chronic renal insufficiency (serum creatinine level 1.3 mg/dL [114.9 µmol/L]) and have received at least 100 mL of contrast medium.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Study Design and Inclusion Criteria
Patients meeting the inclusion criteria were referred to us by the departments of gastroenterology, cardiology, vascular surgery, and urology. A total of 100 consecutive patients with a stable serum creatinine level of 1.3 mg/dL (114.3 µmol/L) or higher were prospectively randomized to receive, by means of a double-blinded method, either 200 mg theophylline (Bronchoparat; Klinge Pharma, Munich, Germany) or a placebo (saline) administered intravenously as a short infusion 30 minutes before at least 100 mL low-osmolarity contrast medium (iomeprol, Imeron 300 or 350; Byk-Gulden, Konstanz, Germany) was administered. In patients undergoing coronary angiography, Imeron 350 was administered; in all other patients, Imeron 300 was used.
Serum creatinine level stability was verified by comparing baseline values obtained immediately before contrast medium application, with at least one value obtained in the preceding 2 days. Patients with a difference greater than 0.3 mg/dL [26.5 µmol/L] were excluded. The stability cutoff of 0.3 mg/dL was chosen as a compromise of the following considerations: (a) The cutoff for stability should be a concentration of serum creatinine above the daily variance in patients with impaired renal function. (b) The cutoff should be a concentration of serum creatinine below the 0.5 mg/dL (44.2 µmol/L) used in Barrett and Parfrey’s (2) definition.
Further exclusion criteria were pregnancy or contraindications for theophylline use such as untreated high-grade arrhythmia or history of seizure.
The use of diuretics or nephrotoxic medications was not restricted. Hydration was performed according to clinical examination findings, radiographic evidence of pulmonary edema, and central venous pressure levels, if available. A fluid supply of at least 2 L/d was advised, but no additional hydration was performed, in order to avoid hyperhydration.
Evaluation Criteria
Serum creatinine and blood urea nitrogen levels were determined once 12–48 hours before ("screening"), immediately before ("baseline"), and 12, 24, and 48 hours after contrast medium administration. The incidence of contrast-induced nephropathy was evaluated by using Barrett and Parfrey’s (2) definition (serum creatinine level increase of at least 0.5 mg/dL [44.2 µmol/L] within 48 hours).
Urinary N-acetyl-ß-glucosaminidase (ß-NAG) excretion was determined 0, 4, 12, and 24 hours after administration of contrast medium.
Risk factors associated with the patients were prospectively identified by using medical history and chart review. Risk factors were exploratively analyzed by using multiple regression analysis (backward selection) with Y = maximum increase of serum creatinine level, as compared with baseline level, within 48 hours, as well as the variables of theophylline use (yes or no), age, weight, body mass index, sex (male: yes or no), diabetes (yes or no), hypertension (yes or no), serum creatinine and blood urea nitrogen level at baseline, intraarterial contrast medium administration (yes or no), impaired cardiac function (yes or no), nephrotoxic medication (yes or no), amount of contrast medium, and Cigarroa quotient at baseline (contrast medium [milliliters] x serum creatinine level [mg/dL] per kilogram of body weight) (6).
Statistical Analysis
Dichotomous parameters (factors such as medications and incidence of contrast-induced nephropathy) were compared by using the 
2 test with a two-sided significance level of .05.
The Wilcoxon test for unpaired samples was used to compare continuous parameters between the treatment groups at baseline. The Wilcoxon test for paired samples was used to compare follow-up levels of serum creatinine and ß-NAG with the respective baseline values in each treatment group. All statistical analyses were performed by using SAS software version 6.12 (SAS Institute, Cary, NC).
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The amount of contrast medium used was more than 150 mL for most of the patients in both the theophylline and placebo groups (Fig 1). The amount of contrast medium was 250–349 mL in 15 patients and was at least 350 mL in 10 patients.
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2 test) (Table 2).
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With a serum creatinine level of nearly 2.0 mg/dL (176.8 µmol/L) and with approximately 200 mL contrast medium, both factors were at levels associated with a high incidence of contrast material–induced nephropathy.
The overall incidence of contrast material–induced nephropathy was 10 (10%) of 100 patients. Of these 10 patients, eight were among the 50 patients receiving a placebo (incidence, eight [16%] of 50 patients) and two were among the 50 patients receiving theophylline (incidence, two [4%] of 50). Comparing incidence in the two treatment groups (eight of 50 vs two of 50) resulted in a significant benefit in the patients receiving theophylline prophylaxis (P = .046; 2 test).
Ninety patients received less than 350 mL of contrast medium (44 received the placebo and 46 received theophylline prophylaxis). Again, the incidence was significantly lower in the patients receiving theophylline (one [2%] of 46), as compared with those receiving a placebo (eight [18%] of 44; P = .014).
Table 3 summarizes the main risk factors and characteristics of the 10 patients who developed contrast material–induced nephropathy. Comparison of those 10 patients with the 90 patients without contrast material–induced nephropathy shows that all 10 (100%) had hypertension (vs 72 [80%] of the 90 patients; not significant [2 test]), nine (90%) of 10 patients had impaired cardiac function (as compared with 46 [51%] of the 90 patients without contrast material–induced nephropathy; P = .019), seven (70%) of 10 patients had a Cigarroa quotient greater than 5.0 (vs 35 [39%] of 90 patients; P = .058); nine (90%) of 10 patients received intraarterial contrast medium (vs 63 [70%] of 90 patients; not significant) and eight (80%) of 10 patients were at least 64 years of age (vs 50 [56%] of 90 patients; P = .094).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The efficacy could be statistically demonstrated in four ways: (a) Reduction of the incidence of contrast-induced nephropathy, (b) prevention of an increase of mean serum creatinine level, (c) reduction of the maximum increase of serum creatinine level in the regression analysis, and (d) prevention of an increase in urinary ß-NAG level.
In addition to our results, several clinical studies (17–20) have shown a benefit of theophylline prophylaxis, although these studies were either small or restricted to sensitive methods such as clearance measurement or time course of proteinuria. Unfortunately, the clinical relevance of these measurements is uncertain, as there are no corresponding data, to our knowledge, regarding mortality or length of hospital stay. The necessity of highly sensitive methods for detecting any theophylline benefit is probably attributable to the fact that the number of risk factors for developing contrast-induced nephropathy was limited in previous studies (17–20), which thus excluded the patients who would benefit most. A similar phenomenon was observed in the low- versus high-osmolarity contrast medium studies (11,12): Despite the cumulative inclusion of more than 2,000 patients, low-osmolarity contrast media were beneficial only in patients with impaired renal function (defined as having a serum creatinine level >1.35 mg/dL [119.3 µmol/L] or creatinine clearance <70 mL/min) or diabetes. Due to the low incidence of contrast-induced nephropathy in patients without renal impairment, at least 400 patients would have to receive low-osmolarity contrast medium to prevent a single case of contrast-induced nephropathy (11).
We therefore investigated patients with severe renal impairment and a large number of risk factors associated with development of contrast-induced nephropathy, including nephrotoxic drugs and predominantly intraarterial administration of high amounts of contrast medium. It is unknown whether our findings can be extrapolated to patients intravenously receiving lower amounts of contrast medium.
Despite our policy of including only high-risk patients, the statistical power of our data might have been increased by including a larger number of patients and/or patients with even more impaired renal function. A serum creatinine level cutoff of 1.3 mg/dL (114.3 µmol/L) to define renal impairment is considered relatively low. Nevertheless, with use of Cockroft and Gault’s (21) formula, the mean weight and age of the patients in the current study show a significantly reduced average creatinine clearance of 59.7 mL/min.
The hydration policy in the patients in the current study was to ensure a sufficient fluid supply of at least 2 L/24 h. Thus, hypohydration of the patients can be excluded for both groups. Since there was no upper limit of hydration, we cannot definitely disprove that the patients in the two groups were hydrated differently (ie, that the patients receiving theophylline were more intensively hydrated than the control subjects). However, there is no evidence for better prophylaxis of contrast-induced nephropathy with hydration of more than 2 L/24 h. In contrast, it is worth noting that hyperhydration with pulmonary edema and emergency ultrafiltration was observed in a recent study (18).
The incidence of contrast-induced nephropathy among the control subjects was high but within the range of that in previous studies including patients with similar renal impairment without prophylaxis. In the study by Tepel et al (13), for example, the incidence among the control subjects was 21%.
The prophylactic effect of theophylline is attributed mainly to its glomerular adenosine antagonism. Contrast media osmotically irritate tubulus cells, leading to increased adenosine triphosphate turnover and subsequent release of adenosine (14,20). In contrast with other tissues in which adenosine can lead to hyperemia, in the kidney it causes vasoconstriction of the vas afferens by way of the adenosine-1 receptor and a reduction in renal plasma flow and glomerular filtration rate (15,16,22–25). Adenosine also briefly stimulates the adenosine-2 receptor, albeit to a lesser degree and mostly in the vas efferens. With increasing renal impairment, the vasoconstrictive adenosine-1 receptor response increasingly outweighs the vasodilative adenosine-2 receptor response (15). In animals with diabetic nephropathy, the vasoconstrictive response to adenosine was 30-fold higher than in control animals without renal impairment (26). This explains the slight prophylactic effects of theophylline in studies including patients without severe renal impairment. Our premise, however, is that the results of theophylline prophylaxis will be most prominent in patients with existing renal impairment. It is not known whether our findings can be extrapolated to patients with lower renal impairment and fewer risk factors.
The theophylline dose required to block renal vascular adenosine receptors is well below that shown to affect renal cyclic nucleotide phosphodiesterase activity (19,24,25). Even the single 200-mg dose in the current study was much greater than the minimum dose for adenosine antagonism. This dose, administered orally 1 hour before the contrast medium, prevented a decrease in creatinine clearance, which was observed in the placebo group (19).
In addition to the predominantly glomerular protective effect of theophylline, the ß-NAG excretion data show that tubular protection also is taking place, correlating with the findings of a recent study (18). The ß-NAG release is highly correlated with the initial tubular damage induced with contrast medium (18,27–30). This tubuloprotective effect is more easily understood in light of the observations of Humes et al (31) and Messana et al (32) that the tubulotoxic effects of contrast media can be augmented with hypoxia. The higher renal blood flow thus protects the tubulus cells.
Another mechanism that may be involved is the direct action of theophylline on reactive oxygen species (33), which are also implicated in the pathogenesis of contrast-induced nephropathy (34,35). This would explain the possible prophylactic role of antioxidants such as acetylcysteine (13). However, the protective effects of acetylcysteine have been shown only for intravenous application of 75 mL of contrast medium, an amount usually not associated with a markedly increased incidence of contrast-induced nephropathy (6,7) and not sufficient for most CT or interventional arteriographic examinations.
As a result of the low amount of contrast medium in the study by Tepel et al (13), the mean Cigarroa quotient (2.4) was much lower than the critical threshold of 5.0 (Table 2) (6). In the current study, theophylline enabled reduction of the incidence of contrast material–induced nephropathy in a high-risk collective with a mean quotient of 5.5.
Another advantage of theophylline is that it was effective as a single infusion 30 minutes before contrast medium administration, whereas acetylcysteine treatment needed to be started 24 hours before contrast medium administration in combination with hydration.
Pathophysiologically, adenosine functions further upstream than do oxygen free radicals in causing contrast-induced nephropathy. In addition to direct glomerular vasoconstriction, adenosine metabolism to xanthin and hypoxanthine increases the generation of oxygen free radicals (36). Methylxanthines such as theophylline and aminophylline are not only adenosine antagonists but are also hydroxyl scavengers (33) and superoxide release inhibitors (37). These effects might contribute to the prophylactic effect of theophylline. To what degree glomeruloprotective adenosine antagonism, tubuloprotection, or antioxidant effects have contributed to the efficacy of theophylline cannot be determined with the results of the current study.
With respect to pathophysiology, as well as our data and that of Tepel et al (13), a combination of theophylline and acetylcysteine might provide better prophylaxis than do either of these agents alone. Twenty patients in the current study received acetylcysteine in low mucolytic doses (600–900 mg/d). However, the distribution of patients receiving acetylcysteine was not different between the control subjects and the theophylline group. Thus, a bias in favor of the theophylline group can be excluded.
The combination of theophylline or acetylcysteine with other preventive approaches may also have cumulative effects. Although, to our knowledge, the prophylactic effect of hydration has not yet been established with a randomized study (38), clinical experience has shown hydration to be a recommended procedure, particularly since any preexistent dehydration can thus be combated. However, hydration with a minimum of 50 mL/h saline must be started at least 12 hours before contrast medium administration. Thus, hydration is of limited use in emergency situations and in patients at risk of hyperhydration.
Studies regarding the use of renal vasodilators such as calcium antagonists (39,40), dopamine (3), atrial natriuretic peptide (9), and endothelin antagonists (41) have shown no or even deleterious effects. Diuretics such as mannitol and furosemide increase the risk of contrast-induced nephropathy (42,43). Prostaglandins (44,45) and angiotensin-converting enzyme, or ACE, inhibitors (46) seem more promising, although, to our knowledge, prevention of contrast material–induced nephropathy according to Barrett and Parfrey’s (2) definition has yet to be demonstrated. Whether and in which patients prophylaxis with acetylcysteine, ACE inhibitors, prostaglandins, or a combination of these agents with theophylline is superior to that with theophylline alone should be the subject of further study. To our knowledge, no controlled evidence is available for postexpositional dialysis with regard to patient outcome. Two small studies (47,48) have not shown any benefit.
In conclusion, among all of the preventive approaches, theophylline is currently the most promising. Including the data from our study with 100 patients, at least five randomized studies with a total of 370 patients (Erley et al [1994] [17], 39 patients and 1999 [18], 80 patients; Katholi et al, 1995 [19], 93 patients; Kolonko et al [1998] [20], 58 patients) have shown significant prophylactic effects, especially in high-risk patients: Theophylline prevented decrease in serum creatinine (17,19,20), inulin, and paraaminohippurate clearance (17). It prevented increase in enzymuria (18,20) and mean serum creatinine levels (20). Most important, in high-risk patients it reduces the incidence of contrast material–induced nephropathy. As compared with other preventive approaches, prophylaxis with 200 mg intravenously administered theophylline 30 minutes before contrast medium administration is straightforward, inexpensive, safe, immediate, and thus useful in emergency situations.
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FOOTNOTES |
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Author contributions: Guarantors of integrity of entire study, W.H., K.I., U.S., L.L., M.C.; study concepts, W.H., K.I., B.J., M.P., W.W., U.S.; study design, W.H., K.I., B.J., M.P., W.W., U.S., H.S., M.C.; literature research, W.H., K.I., B.J., M.P., U.S., H.S.; clinical studies, W.H., K.I., L.L., M.H., B.J., M.P., W.W., U.S., H.S.; experimental studies, W.H., K.I., L.L., M.P., W.W., U.S.; data acquisition, W.H., K.I., M.H., L.L., B.J., M.P., W.W., U.S., H.S.; data analysis/interpretation, W.H., K.I., M.H., B.J., M.P., H.S., W.W., U.S.; statistical analysis, M.H., W.H., K.I.; manuscript preparation, all authors; manuscript definition of intellectual content, W.H., K.I., M.P., B.J., H.S., W.W., U.S., K.I., M.C.; manuscript editing, W.H., K.I., M.P., M.H., B.J., U.S., H.S.; manuscript revision/review and final version approval, all authors.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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= greater than 1.5 x IQR beyond the quartiles; x = greater than 3.0 x IQR beyond the quartiles; solid box = 12 hours to baseline; cross-hatched boxes = 24 hours to baseline; boxes with diagonal lines = 48 hours to baseline. (To convert serum creatinine values to micromoles per liter, multiply by 88.4).