Prevention of Contrast-Induced Nephropathy
Prevention of Contrast-Induced Nephropathy
Author: Elizabeth W. Kelly, MD, Clinical Instructor of Emergency Medicine, Wake Forest University Baptist Medical Center, Winston-Salem, NC; and James O'Neill, MD, Assistant Director, Undergraduate Medical Education, Wake Forest University Baptist Medical Center, Winston-Salem, NC.
Peer Reviewer: Christine B. Irish, MD, FACEP, Director of Emergency Ultrasound, Department of Emergency Medicine, Maine Medical Center, Portland, ME.
Introduction
Contrast-induced nephropathy (CIN) is a typically reversible form of acute renal insufficiency that occurs after the administration of IV contrast. While it usually resolves quickly, a certain percentage of patients will go on to have renal insufficiency or failure. CIN is generally defined by a proportional rise of 25% in serum creatinine or an absolute increase in creatinine by 0.5mg/dL from baseline 48 hours after contrast exposure.1,2 Preexisting renal dysfunction and diabetes mellitus are both independent predictors of CIN.3,4 Studies also suggest that comorbidities such as congestive heart failure, hypertension, and peripheral vascular disease are associated with the condition.5
There are two main theories to explain the pathogenesis of CIN. The first is that contrast induces renal vasoconstriction resulting in medullary hypoxemia.6 This mechanism is likely mediated by nitric oxide, endothelin, and/or adenosine.6 The second is that acute tubular injury results from direct cytotoxic effects of the contrast and/or from the generation of oxygen free radicals.7-12
The reported incidence of CIN varies widely but in the general population it is low, between 0.7%13 and 3.3%.14 However, patients with creatinine levels above the hospital's upper limit of normal or with an estimated GFR< 60 have an incidence greater than 30%.3,14,15 Studies indicate that the incidence has not changed much in the last three decades, and that it continues to be the third leading cause of hospital-acquired acute renal failure.16
A wide range of treatment protocols and agents have been studied in search of ways to prevent CIN. The objective of this article will be to focus on interventions that may be considered in an acute care setting.
Sodium Bicarbonate: Useful in Preventing CIN in an Acute Care Setting?
Sources: Merten GJ, Burgess WP, Gray LV, et al. Prevention of contrast-induced nephropathy with sodium bicarbonate: A randomized controlled trial. JAMA 2004;291:2328-2334; Masuda M, Yamada T, Mine T, et al. Comparison of usefulness of sodium bicarbonate versus sodium chloride to prevent contrast-induced nephropathy in patients undergoing an emergent coronary procedure. Am J Cardiol 2007;100:781-786; Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs. sodium chloride for the prevention of contrast medium-induced nephropathy in patients undergoing coronary angiography: A randomized trial. JAMA 2008;300:1038-1046.
Merten and colleagues examined the efficacy of sodium bicarbonate compared with sodium chloride for preventive hydration before and after radiographic contrast. They performed a prospective, single-center, randomized trial of 119 patients. Patients received either sodium chloride or sodium bicarbonate as a bolus of 3 mL/kg per hour for 1 hour before contrast, followed by an infusion of 1 mL/kg per hour for 6 hours after the procedure. They found CIN occurred in eight patients (13.6%) who received sodium chloride but in only one (1.7%) of those who received sodium bicarbonate. They had planned to enroll 260 patients to find a statistically significant difference with a power of 80%; however, they stopped the study early due to ethical concern about continuing to expose the sodium chloride group to the higher risk of CIN. They concluded that hydration with sodium bicarbonate is more effective than hydration with sodium chloride for CIN prophylaxis.
Masuda and colleagues also studied hydration with sodium chloride vs. sodium bicarbonate in patients undergoing an emergency coronary procedure for suspected acute coronary syndrome. Their study group included patients defined as having chronic kidney dysfunction (CKD) (creatinine > 1.1mg/dL or glomerular filtration rate < 60) 59 patients were enrolled in this single institution prospective, randomized controlled trial. The same infusion protocol as in the previously discussed Merten study was used. They found that serum creatinine remained unchanged in the sodium bicarbonate group within two days post-contrast, whereas it increased in the sodium chloride group. They also found the incidence of CIN to be lower in the sodium bicarbonate group, 7% vs. 35%. Just as in the Merten study, the study was terminated early because of ethical concern. They concluded that hydration with sodium bicarbonate is more effective at preventing CIN in this high-risk group of patients.
In 2008 Brar and colleagues published a study similar to that of Masuda's group, with 353 patients with CKD who were undergoing coronary intervention. This was a large, single-blinded, randomized controlled trial comparing hydration with sodium bicarbonate vs. sodium chloride. These patients had a GFR of 60 or less and one or more of the following co-morbid conditions: diabetes, history of congestive heart failure, hypertension, or age older than 75 years. The infusion protocol was slightly different than the Masuda and Merton studies. Patients received 3 mL/kg of sodium bicarbonate for 1 hour before coronary angiography, decreased to 1.5 mL/kg per hour during the procedure, and further decreased to 1 mL/kg per hour for 4 hours after completion of the procedure. In contrast to the first two studies, they found no difference in the incidence of CIN between the two groups.
Commentary
It is widely accepted that hydration is protective against CIN, but there is significant debate as to whether hydration with sodium bicarbonate is superior to hydration with sodium chloride. There are two proposed mechanisms that support hydration with sodium bicarbonate. Merten and colleagues suggested that sodium bicarbonate might decrease free radical formation by increasing the pH of the renal tubule and therefore decreasing tubular injury.17 Additionally, there is some evidence that sodium bicarbonate acts as a scavenger of peroxynitrate, which is a potent oxidant produced via a nitric oxide-mediated pathway.18 A reduction in peroxynitrate would therefore decrease the toxicity to tubular cells.
The discordant results of these three studies suggests that more research is necessary before changing clinical practice. All three studies had limitations that should be noted. Since the clinical trials conducted by the Merten and Masuda groups were terminated early, this may have led to an overestimation of the treatment effect given natural random fluctuations in randomized controlled trials.19-21 On the flip side, a large portion of the Brar patients were treated with N-acetylcysteine (NAC) 24 hours before contrast, and those who did not receive NAC were a healthier subgroup, which may have resulted in an underestimation of the effect of bicarbonate.
Until further trials are conducted, it should be noted that the use of sodium bicarbonate may decrease the risk of CIN in select patient populations. It is a low-cost, low-risk prophylactic agent22 that could be practical for use in an acute care setting and requires pretreatment only one hour before contrast injection.
Is NAC Useful in Preventing CIN in an Acute Care Setting?
Sources: Ochoa A, Pellizzon G, Addala S, et al. Abbreviated dosing of N-acetylcysteine prevents contrast-induced nephropathy after elective and urgent coronary angiography and intervention. J Interv Cardiol 2004;17:159-165; Baker CS, Wragg A, Kumar S, et al. A rapid protocol for the prevention of contrast-induced renal dysfunction: The RAPPID study. J Am Coll Cardiol 2003;41:2114-2118; Durham JD, Caputo C, Dokko J, et al. A randomized controlled trial of N-acetylcysteine to prevent contrast nephropathy in cardiac angiography. Kidney Int 2002;62: 2202-2207.
Ochoa and colleagues performed a prospective, randomized controlled trial of a short, high-dose regimen of N-acetylcysteine (NAC) in patients with chronic renal insufficiency undergoing urgent or emergency percutaneous coronary intervention (PCI). Since lengthy pretreatment was not possible with these patients, a dosing of 1,000 mg 1 hour before and 1,000 mg 4 hours after PCI was tested against a placebo. All patients received 150 ml/hour of normal saline (NS) for 4 hours before and 6 hours after the procedure. CIN was defined in this study as increase in creatinine of 0.5 mg/dL or 25% in the 48 hours following PCI. Of the 80 patients in this study, 3/36 (8%) of the treatment arm and 11/44 (25%) of the placebo arm developed CIN (P= 0.051).
Baker and colleagues performed a prospective, randomized controlled trial of intravenous NAC in patients undergoing PCI. This study compared NAC with NS versus placebo with NS alone. The patients all had a serum creatinine of > 1.36 or a creatinine clearance of < 50 mL/min at baseline and the study was not blinded. The patients were randomized at enrollment; one arm received 150 mg/kg of NAC in NS over 30 minutes before the procedure and 50 mg/kg of NAC in NS in the subsequent 4 hours. The other placebo arm received 1 mL/kg/hour of NS for 12 hours preprocedure and 12 hours postprocedure. CIN was determined by a 25% increase in serum creatinine in values measured either 48 or 96 hours post procedure. All patients had diuretics and ACE inhibitors held for 24 hours before the procedure, and patients with non-steroidal anti-inflammatory use within 24 hours of PCI were excluded. The authors found that 2/41 patients (5% in the NAC arm developed CIN, as compared to 8/39 patients (21%) in the placebo arm (P=0.045).
Durham and colleagues performed a prospective, randomized controlled trial that compared intravenous hydration plus NAC versus intravenous hydration plus placebo in patients undergoing PCI. Patients were eligible for this study if their baseline serum creatinine was > 1.7 mg/dL. CIN was defined as an increase of serum creatinine by 0.5 mg/dL or more. All patients received hydration with 1 mL/kg/hour of 0.45% NS for 12 hours pre-procedure and 12 hours post-procedure. Oral NAC was administered 1 hour before and 3 hours after the procedure. This study did not show a significant difference in the two treatment groups, as CIN occurred in 26.3% of the NAC group and 22% of the placebo group.
Commentary
The study by Ochoa and colleagues was limited by its small sample size and the poor follow-up in obtaining the 48-hour post-procedure creatinine. In fact, only 80 of 105 patients randomized in this trial were included in the final data due to lack of creatinine testing at the predetermined study times. Patients in both study arms received at least 500 mL of NS 12 hours before the procedure and at least 1,000 mL in the 24 hours after the procedure. However, it is possible that the patients in either arm could have received a significantly larger amount of intravenous NS and these amounts were not reported in the study. It is difficult to endorse this protocol in light of these study limitations.
The study by Baker and colleagues also suffer from several limitations. The study design is flawed since it did not compare the use of NAC to a true placebo. Patients in the control group received NS for 12 hours before and 12 hours after the study. In addition, the NAC group received 1 liter of NS one hour before the contrast was given. The placebo group received the initial 1 liter over 12 hours. This is a significant difference and could contribute to the different results between groups. Finally, most patients in the emergency department have not held their nephrotoxic medications for 24 hours before testing and intravenous NAC may not be available for all emergency physicians.
The study by Durham's team was limited by its small sample size and results that were not statistically significant. Combined, these studies do not provide enough evidence to recommend NAC as prophylaxis for CIN. The studies are complicated by the different rates and amounts of IV NS administered to study patients and small sample sizes. Furthermore, these results (rise in serum creatinine) do not measure whether the administration of NAC impacts clinically significant endpoints, such as progression to renal failure, dialysis, or death.
What about Theophylline as CIN Prophylaxis?
Source: Bagshaw SM, Ghali WA. Theophylline for prevention of contrast induced nephropathy: A systematic review and meta-analysis. Arch Intern Med 2005;165:1087-1093.
Bagshaw, et al performed a systematic review and meta-analysis and identified nine randomized trials involving 585 patients treated with various protocols of theophylline for the prevention of CIN. Results differed extensively across trials, and therefore the authors were cautious about their pooled odds ratio of 0.40 (95% confidence interval, 0.14-0.16; P=0.09), which indicated a trend toward reduction of CIN. The overall pooled estimate for the difference in 48-hour serum creatinine levels between the theophylline and control groups was -0.17 mg/dL (95% CI, -0.28 to -0.06 mg/dL) (-15.2 µmol/L [95% CI, -24.6 to -5.7 µmol/L]) (P = 0.002), which suggested that theophylline may have a protective effect against CIN.
Commentary
Adenosine has been proposed to contribute to CIN, and therefore theophylline, an adenosine antagonist, has been study extensively as a possible protective agent.23 Theophylline use is limited by its significant side-effect profile, including ventricular arrhythmias, seizures, and shock.7 The results of this meta-analysis of theophylline use were inconclusive. Given the serious side effects, the routine use of theophylline for CIN prevention is not recommended.
What about Ascorbic Acid as CIN Prophylaxis?
Sources: Spargias K, Alexopoulos E, Kyrzopoulos S, et al. Ascorbic acid prevents contrast-mediated nephropathy in patients with renal dysfunction undergoing coronary angiography or intervention. Circulation 2004;110:2837-2842; Boscheri A, Weinbrenner C, Botzek B, et al. Failure of ascorbic acid to prevent contrast-media induced nephropathy in patients with renal dysfunction. Clin Nephrol 2007;68:279-286.
Spargias and colleagues performed a randomized, double-blind, placebo-controlled trial of 231 patients with an elevated baseline creatinine who were undergoing coronary intervention. Three grams of ascorbic acid were administered at least 2 hours before the procedure and 2 grams were administered that night and again the morning after the procedure. CIN occurred in 9% of the ascorbic acid group and 20% of the placebo group (odds ratio [OR], 0.38; 95% confidence interval [CI], 0.17 to 0.85; P = 0.02). They also found that the mean creatinine increased significantly in the placebo group and nonsignificantly in the ascorbic acid group. The mean increase in creatinine was also greater in the placebo group (difference of 0.09 mg/dL; 95% CI, 0.00 to 0.17; P = 0.049). They concluded that ascorbic acid may prevent CIN in this group of high-risk patients.
Boscheri et al evaluated the efficacy of ascorbic acid as an adjunct to hydration in preventing CIN after coronary procedures. They enrolled 143 consecutive patients with a creatinine > 1.2 who were scheduled to undergo coronary angiography. The study design was a randomized, double-blind, prospective, single center-study where patients received 1 g ascorbic acid or placebo in adjunct to saline hydration prior to and after angiography. CIN occurred in 8/143 (5.6%) of all patients. No significant difference in CIN incidence was detected between study groups (vitamin C 5/74 [6.8%] patients; placebo 3/69 [4.3%] patients). These authors do not support the prophylactic use of ascorbic acid in this high-risk patient population.
Commentary
Given the antioxidative properties of ascorbic acid,24 it has been advocated as a possible preventative measure against CIN. The studies by Boscheri and Spargias had conflicting conclusions regarding its role in CIN prevention. It is important to note that the Spargias trial was a small, single-center study that used the least stringent definition of CIN (25% proportional increase in creatinine). Therefore, given these limitations and the lack of support from other studies, including that of Boscheri and colleagues, ascorbic acid is not recommended as first-line prevention for CIN.
Summary
The wide variation in overall reported incidence of CIN results from many factors, including the differences in the definition, presence, or absence of risk factors, and amount and type of contrast used. The decision regarding which type of contrast agent to administer is usually not the responsibility of the acute care provider, but rather is predetermined by hospital protocols or radiology department guidelines. Large clinical studies and meta-analyses have shown decreased incidence of CIN in high-risk patients when a low-osmolar contrast medium is used as compared to a high-osmolar medium.25-30 Data also suggests that iso-osmolar contrast media are even less nephrotoxic than low-osmolar agents, presumably due to the osmolality, the chemotoxicity, or their ionic composition.31-33 Therefore, it is important for emergency providers to be aware of the types of contrast used in their facility and the alternatives available to them. In the event of a high-risk patient with CKD and diabetes, requesting the use of an iso-osmolar agent may be an option to help reduce the incidence of CIN.34
The incidence of acute renal failure requiring dialysis due to CIN appears to be quite low. A retrospective review of 58,000 patients undergoing coronary procedures found less than 0.1% required dialysis within a month of the procedure. It was not clear whether this could be attributed to the contrast load or instead due to alternative causes such as hypotension or embolic disease.35 Other studies have failed to demonstrate a significant rate of CIN. A recent retrospective comparison of 11,588 patients showed no significant difference in creatinine elevation between those receiving contrast vs. those undergoing unenhanced CTs.36 Clearly, despite the significant research on CIN, the controversy continues regarding incidence, etiology, and appropriate preventive measures.
There are additional factors that can limit research in CIN. Certain medications may spuriously elevate the serum creatinine levels. The antibiotic trimethoprim- sulfamethoxazole and the H2-blocker cimetidine are two commonly used drugs that decrease the secretion of creatinine, resulting in a self-limited and reversible increase in the serum creatinine level of as much as 0.4-0.5 mg/dL.37 To a lesser degree, famotidine and ranitidine can temporarily elevate serum creatinine, and cefoxitin interferes with the assay used to measure serum creatinine levels, causing a false elevation.37 The use of these medications can complicate research in CIN.
Despite the ongoing controversies on the topic, it is clear that there is increasing reliance on CT scans in emergency departments and other acute care settings.38 Therefore, prevention of CIN is becoming more relevant to emergency providers. The literature has consistently shown a reduction in long-term survival of patients who develop CIN, both during the short-term period of hospitalization and for up to a year or more following illness.39 Since treatment is limited to supportive care, emphasis should be placed on preventative measures, identifying high-risk patients, and educating all physicians caring for these patients.40
Regarding CIN preventative modalities, review Table 1 for a quick summary of the agents discussed here. Note that these recommendations are for use in high-risk patients; i.e., those with chronic kidney dysfunction and/or diabetes mellitus.
 |
In summary, sodium bicarbonate is an acceptable prophylactic agent that is very low risk and may reduce the incidence of CIN in high-risk patients. NAC may be of benefit if used well in advance, but is not practical for an acute care setting. The evidence to support theophylline is inconclusive, and given its high-risk side effect profile, it is currently not recommended as first-line prophylaxis. Although it is a low-risk agent, the data to support ascorbic acid is inconclusive, and it should not be used as first-line prophylaxis. Evidence supports the use of iso-osmolar agents over low-osmolar or high-osmolar agents when possible in high-risk patients.
One of the most effective ways to prevent CIN is to identify high-risk patients, namely those with chronic kidney dysfunction and/or diabetes, and to limit the use of IV contrast in these patients. Ongoing dialogue with radiology is also recommended to identify alternative diagnostic tests, such as unenhanced CTs, ultrasound, or MRI. When IV contrast is absolutely necessary in high-risk patients, adequate hydration, limiting the amount of contrast, and choice of contrast agent are of utmost importance.
References
1. Barrett BJ, Parfrey PS. Clinical practice. Preventing nephropathy induced by contrast medium. N Engl J Med 2006;354: 379-386.
2. Barrett BJ, Parfrey PS. Prevention of nephrotoxicity induced by radiocontrast agents. N Engl J Med 1994;331:1449-1450.
3. McCullough PA, Wolyn R, Rocher LL, et al. Acute renal failure after coronary intervention: Incidence, risk factors, and relationship to mortality. Am J Med 1997;103:368-375.
4. Mehran R, Aymong ED, Nikolsky E, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: Development and initial validation. J Am Coll Cardiol 2004;44:1393-1399.
5. Bartholomew BA, Harjai KJ, Dukkipati S, et al. Impact of nephropathy after percutaneous coronary intervention and a method for risk stratification. Am J Cardiol 2004;93:1515-1519.
6. Persson PB, Hansell P, Liss P. Pathophysiology of contrast medium-induced nephropathy. Kidney Int 2005;68:14-22.
7. Pflueger A., Larson TS, Nath KA, et al. Role of adenosine in contrast media-induced acute renal failure in diabetes mellitus. Mayo Clin Proc 2000;75:1275-1283.
8. Russo D, Minutolo R, Cianciaruso B, et al. Early effects of contrast media on renal hemodynamics and tubular function in chronic renal failure. J Am Soc Nephrol 1995;6:1451-1458.
9. Katholi RE, Taylor GJ, McCann WP, et al. Nephrotoxicity from contrast media: Attenuation with theophylline. Radiology 1995;195:17-22.
10. Cantley LG, Spokes K, Clark B, et al. Role of endothelin and prostaglandins in radiocontrast-induced renal artery constriction. Kidney Int 1993;44:1217-1223.
11. Weisberg LS, Kurnik PB, Kurnik BR. Radiocontrast-induced nephropathy in humans: Role of renal vasoconstriction. Kidney Int 1992;41:1408-1415.
12. Agmon Y, Peleg H, Greenfeld Z, et al. Nitric oxide and prostanoids protect the renal outer medulla from radiocontrast toxicity in the rat. J Clin Invest 1994;94:1069-1075.
13. Davidson CJ, Hlatky M, Morris KG, et al. Cardiovascular and renal toxicity of a nonionic radiographic contrast agent after cardiac catheterization. A prospective trial. Ann Intern Med 1989;110:119-124.
14. Rihal CS, Textor SC, Grill DE, et al. Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention. Circulation 2002;105:2259-2264.
15. Gruberg L, Mintz GS, Mehran R, et al. The prognostic implications of further renal function deterioration within 48 h of interventional coronary procedures in patients with pre-existent chronic renal insufficiency. J Am Coll Cardiol 2000;36:1542-1548.
16. Finn WF. The clinical and renal consequences of contrast-induced nephropathy. Nephrol Dial Transplant 2006;21:i2-10.
17. Merten GJ, Burgess WP, Gray LV, et al. Prevention of contrast-induced nephropathy with sodium bicarbonate: A randomized controlled trial. JAMA 2004;291:2328-2334.
18. Caulfield JL, Singh SP, Wishnok JS, et al. Bicarbonate inhibits N-nitrosation in oxygenated nitric oxide solutions. J Biol Chem 1996;271:25859-25863.
19. Heffner AC, Milbrandt EB, Venkataraman R. Trials stopped early for benefit? Not so fast! Crit Care 2007;11:305.
20. Bassler D, Ferreira-Gonzalez I, Briel M, et al. Systematic reviewers neglect bias that results from trials stopped early for benefit. J Clin Epidemiol 2007;60:869-873.
21. Sinert R, Doty CI. Update: Prevention of contrast-induced nephropathy in the emergency department. Ann Emerg Med 2009;54:e1-5.
22. Sinert R, Doty CI, Brown MD. Bicarbonate to prevent contrast-induced nephropathy in the emergency department: Does the Brar study change recommendations? Ann Emerg Med 2009; 54:e6-7.
23. Bagshaw SM, Ghali WA. Theophylline for prevention of contrast-induced nephropathy: A systematic review and meta-analysis. Arch Intern Med 2005;165:1087-1093.
24. Briguori C, Airoldi F, D'Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): A randomized comparison of 3 preventive strategies. Circulation 2007;115:1211-1217.
25. Barrett BJ, Carlisle EJ. Metaanalysis of the relative nephrotoxicity of high- and low-osmolality iodinated contrast media. Radiology 1993;188:171-178.
26. Barrett BJ. Contrast nephrotoxicity. J Am Soc Nephrol 1994;5: 125-137.
27. Lautin EM, Freeman NJ, Schoenfeld AH, et al. Radiocontrast-associated renal dysfunction: A comparison of lower-osmolality and conventional high-osmolality contrast media. AJR Am J Roentgenol 1991; 157:59-65.
28. Wang A, Holcslaw T, Bashore TM, et al. Exacerbation of radiocontrast nephrotoxicity by endothelin receptor antagonism. Kidney Int 2000;57:1675-1680.
29. Taliercio CP, Vlietstra RE, Ilstrup DM, et al. A randomized comparison of the nephrotoxicity of iopamidol and diatrizoate in high risk patients undergoing cardiac angiography. J Am Coll Cardiol 1991;17:384-390.
30. Rudnick MR, Goldfarb S, Wexler L, et al. Nephrotoxicity of ionic and nonionic contrast media in 1196 patients: A randomized trial. The Iohexol Cooperative Study. Kidney Int 1995;47:254-261.
31. Berg KJ. Nephrotoxicity related to contrast media. Scand J Urol Nephrol 2000;34:317-322.
32. Morcos SK. Contrast media-induced nephrotoxicity-Questions and answers. Br J Radiol 1998;71:357-365.
33. Katzberg RW. Urography into the 21st century: New contrast media, renal handling, imaging characteristics, and nephrotoxicity. Radiology 1997;204:297-312.
34. Aspelin P, Aubry P, Fransson SG, et al. Nephrotoxic effects in high-risk patients undergoing angiography. N Engl J Med 2003;348:491-499.
35. Liss P, Persson PB, Hansell P, et al. Renal failure in 57,925 patients undergoing coronary procedures using iso-osmolar or low-osmolar contrast media. Kidney Int 2006;70:1811-1817.
36. Bruce R.J, Djamali A, Shinki K, et al. Background fluctuation of kidney function versus contrast-induced nephrotoxicity. AJR Am J Roentgenol 2009;192:711-718.
37. Paige NM, Nagami GT. The top 10 things nephrologists wish every primary care physician knew. Mayo Clin Proc 2009;84: 180-186.
38. Boone JM, Brunberg JA. Computed tomography use in a tertiary care university hospital. J Am Coll Radiol 2008;5:132-138.
39. Rudnick M, Feldman H. Contrast-induced nephropathy: What are the true clinical consequences? Clin J Am Soc Nephrol, 2008;3:263-272.
40. Newhouse JH, Kho D, Rao QA, et al. Frequency of serum creatinine changes in the absence of iodinated contrast material: Implications for studies of contrast nephrotoxicity. AJR Am J Roentgenol 2008;191:376-382.
Contrast-induced nephropathy (CIN) is a typically reversible form of acute renal insufficiency that occurs after the administration of IV contrast.Subscribe Now for Access
You have reached your article limit for the month. We hope you found our articles both enjoyable and insightful. For information on new subscriptions, product trials, alternative billing arrangements or group and site discounts please call 800-688-2421. We look forward to having you as a long-term member of the Relias Media community.