Contrast-Induced Nephropathy in an Intensive Care Setting

Fatima I Al-Beladi

Department of Internal Medicine, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia*

Corresponding Author: Fatima I Al-Beladi, Department of Internal Medicine, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia. Tel: +966(012)6408243, Fax: +966(012)6408315, Email:
Published on 26th June, 2015


Contrast-induced nephropathy (CIN) is an increasingly common cause of acute kidney injury due to the growing use of contrast media for diagnostic and therapeutic intervention. Although critically ill patients, a population who may be particularly vulnerable to CIN, its prevalence and impact in this population has not been the focus of much research. We conducted a prospective study to examine the prevalence of CIN in an intensive care unit (ICU) population and to determine its impact on patients’ outcome. In total, 84 patients were admitted to the ICU and received computed tomography scan or non-coronary angiography with intravenous administration of iodinated contrast media between January 2010 and December 2011. Patients were observed for 72 h post-contrast. During this period, 21 patients (25.0%) developed CIN. Development of CIN was not related to age, gender, body mass index, baseline creatinine, or urinary output. In patients developing CIN, baseline cystatin C levels were significantly higher than in those who did not develop CIN (P=0.012). There was significantly higher mortality in CIN patients (76.0% vs. 46.0%; P=0.038). No differences were found in hospital or ICU length of stay. CIN occurred relatively frequently in our ICU population and had a significant impact on patient outcome. Future work should seek to identify risk factors and early markers for the detection of CIN.

Key words: Computed Tomography Scan, Non-Coronary Angiography, Intravenous Administration, Iodinated Contrast Media



Contrast-induced nephropathy (CIN) has been reported as the third most common cause of acute kidney injury (AKI) in hospitalized patients.1 CIN is associated with increased hospital duration of stay, mortality, and healthcare costs.2 A recent study found that mortality was 5-fold higher (31% vs. 6%) in hospitalized patients who received contrast media and developed CIN compared to those that did not develop CIN.3

Although there has been much research on CIN outside of the intensive care unit (ICU), little research has been conducted on CIN in ICU patients. Given that ICU patients may be particularly vulnerable to CIN due to multiple acute cerebral ischemic risk factors, understanding the prevalence, and impact of CIN on this patient population is important. Moreover, since critically ill patients have a poor prognosis from AKI,4 it is likely that CIN will have particularly high mortality and morbidity in this population.

In this prospective study, we sought to examine the prevalence of CIN in intensive care patients and to determine its impact on patient’s outcome.


Materials and Methods


We conducted a prospective single-center study on all patients who were admitted to the ICU of King Abdulaziz University Hospital who had undergone diagnostic computed tomography (CT) scan or non-coronary angiography with intravenous administration of iodinated contrast media during the period from January 2010 to December 2011. King Abdulaziz University Hospital is a 26-bed hospital with an ICU that consists of a 10-bed adult surgical ICU and a 16-bed medical ICU. Prior to their inclusion in the study consent was obtained from all participants. Study approval was granted by the Biomedical Ethics Research Committee of King Abdulaziz University.

All patients aged between 18 and 75 years who were admitted to the ICU and who were scheduled for diagnostic CT or non-coronary angiography with intravenous administration of iodinated contrast media were included in the study. We excluded all patients younger than 18 years or older than 75, patients who had heart failure, pregnant women, patients on dialysis, patients who had received intravenous contrast within 72 h before the start of the study, patients known to have an allergy to contrast products, those undergoing cardiac catheterization, and those with end stage renal disease.

We collected demographic data of all the patients included in the study, including age and gender, and we recorded the admission diagnosis, co-morbidities, acute physiology and chronic health evaluation II (APACHE-II), and sepsis-related organ failure assessment (SOFA) scores to assess the severity of the illness upon ICU admission. We also recorded ICU mortality. RIFLE criteria were determined at admission. In line with previous studies, we used the lowest creatinine level found within 3 months prior to ICU admission as a baseline for the individual creatinine-based RIFLE classification.5 When no true pre-admission creatinine existed, the admission creatinine level was used.

Laboratory investigations, including urea, creatinine, serum electrolytes, cystatin C, and lactic acid were performed as part of routine patient care. Urine output was measured on an hourly basis after admission. Blood sampling for cystatin C measurements was performed on inclusion into the study. Samples were centrifuged at 4000 rpm for 6 min. The supernatants were stored at −80°C until assayed batchwise. Cystatin C was measured with a particle-enhanced immunonephelometric method on a Dimension Vista Analyzer (Siemens, Newark, DE19714, USA). Levels of urea and creatinine were measured by standard chemical and clinical methods.

Patients were classified as developing CIN if their creatinine levels increased by more than 25% or 44 mmol/L from their baseline measurement.

Statistical Analysis

Data was entered in excel and analyzed using SPSS version 19.0 for Windows (SPSS, Chicago, IL, USA). Demographic characteristics are presented for continuous variables as means and standard deviations and categorical variables as frequencies and percentages. CIN and non-CIN patients were compared using the Chi-square test for categorical variables and Student’s t-test for continuous variables. Significance was set at the 0.05 level.



A total of 84 patients were included in the study. Common diagnoses included diabetes mellitus and hypertension (n=14; 16.7%) and cancer (n=13; 15.6%). During the 72 h post-contrast follow-up period, 21 patients (25.0%) developed CIN. Of these, 14 (66.7% of those developing CIN) developed CIN on day 1, 4 (19.0%) developed CIN on day 2, and 3 (14.3%) developed CIN on day 3.

No significant differences were found in age and body mass index in those that developed CIN compared to those that did not develop CIN (Table 1). Male and female patients were equally likely to develop CIN. The median baseline APACHE-II score was 20 (range 7-31) in CIN patients and 18 (range 7-31) in non-CIN patients, while the median baseline SOFA score was 6 (range 2-13) in both groups. Patients with sepsis, diabetes mellitus, hypertension, and ischemic heart disease were equally likely to develop CIN than to not develop CIN (Table 1).

Table 1. Baseline characteristics


Measurement of creatinine, urea and urinary output at baseline could not distinguish between those that developed CIN and those that did not (Table 2). Similarly, no differences were found in baseline sodium, potassium, and lactate levels between the two groups. However, cystatin C levels were significantly higher (P=0.012) at baseline in patients that developed CIN compared to patients that did not develop CIN.

Table 2. Baseline serum and urinary markers


No significant difference was found in the hospital or ICU lengths of stay for patients developing CIN compared to those who did not (Table 3). However, CIN patients were significantly more likely to require dialysis during their stay (P<0.001) and had a significantly higher incidence of death (P=0.038).

Table 3. Comparison of outcome in patients developing CIN compared to those who did not develop CIN




In this prospective study of ICU patients, we found a relatively high rate of CIN following diagnostic CT or non-coronary angiography with intravenous administration of iodinated contrast media. Our results are comparable with previous studies, which have suggested that the incidence of CIN ranges from 2% to 21% depending on the contrast agent used.6-10

We did not identify any patient factors, such as age, gender, or diagnosis, which were related with the development of CIN. This is in contrast to a recent study which found a significant association between age and CIN.3 However, we did find a significant association between baseline cystatin C levels and the development of CIN. Recent studies have suggested that early detection of AKI may be improved by the use of cystatin C.11-14 Our study also suggests that CIN may be detected using cystatin C.

In line with previous studies, mortality was significantly higher in those developing CIN compared to the non-CIN patients.3 No differences in length of stay were identified, although this may in part be a reflection of the considerable higher mortality rates in the CIN population.

Our study does have limitations. Since all ICU patients were exposed to contrast media, our study lacks a control group, which would allow non-contrast factors affecting outcome to be assessed. In addition, we did not record a number of major risk factors for AKI, including nephrotoxic medications, intravascular volume status, or the reason for the CT scan or non-coronary angiography. A comprehensive risk factor analysis could therefore not be performed.



In summary, CIN-incidence was high in our ICU population and was associated with considerable mortality. Differences in cystatin C levels between the two groups before contrast administration suggest that cystatin C represents a useful marker for predicting the development of CIN. Future studies to further explore potential CIN risk factors and develop early detection biomarkers are necessary, particularly in the setting of ICU.

End Note

Author Information

Fatima I Al-Beladi, Department of Internal Medicine, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia. Tel: +966(012)6408243, Fax: +966(012)6408315, Email:


Conflict of Interest

None declared.


1. Nash K, Hafeez A, Hou S, Hospital-acquired renal insufficiencyAm J Kidney Dis 2002; 39: 930-6. [CrossRef] [PubMed]

2. McCullough PA, Acute kidney injury with iodinated contrastCrit Care Med 2008; 36: S204-11. [CrossRef] [PubMed]

3. Rashid AH, Brieva JL, Stokes B, Incidence of contrast-induced nephropathy in intensive care patients undergoing computerised tomography and prevalence of risk factorsAnaesth Intensive Care 2009; 37: 968-75. [PubMed]

4. Hoste EA, Schurgers M, Epidemiology of acute kidney injury: How big is the problem?Crit Care Med 2008; 36: S146-51. [CrossRef] [PubMed]

5. Mårtensson J, Bell M, Oldner A, Xu S, Venge P, Martling CR, Neutrophil gelatinase-associated lipocalin in adult septic patients with and without acute kidney injuryIntensive Care Med 2010; 36: 1333-40. [CrossRef]

6. Becker CR, Reiser MF, Use of iso-osmolar nonionic dimeric contrast media in multidetector row computed tomography angiography for patients with renal impairmentInvest Radiol 2005; 40: 672-5. [CrossRef]

7. Weisbord SD, Mor MK, Resnick AL, Hartwig KC, Palevsky PM, Fine MJ, Incidence and outcomes of contrast-induced AKI following computed tomographyClin J Am Soc Nephrol 2008; 3: 1274-81. [CrossRef] [PubMed] [PMC Free Article]

8. Tepel M, van der Giet M, Schwarzfeld C, Laufer U, Liermann D, Zidek W, Prevention of radiographic-contrast-agent-induced reductions in renal function by acetylcysteineN Engl J Med 2000; 343: 180-4. [CrossRef] [PubMed]

9. Harjai KJ, Raizada A, Shenoy C, Sattur S, Orshaw P, Yaeger K, A comparison of contemporary definitions of contrast nephropathy in patients undergoing percutaneous coronary intervention and a proposal for a novel nephropathy grading systemAm J Cardiol 2008; 101: 812-9. [CrossRef] [PubMed]

10. Nguyen SA, Suranyi P, Ravenel JG, Randall PK, Romano PB, Strom KA, Iso-osmolality versus low-osmolality iodinated contrast medium at intravenous contrast-enhanced CT: Effect on kidney functionRadiology 2008; 248: 97-105. [CrossRef] [PubMed]

11. Wald R, Liangos O, Perianayagam MC, Kolyada A, Herget-Rosenthal S, Mazer CD, Plasma cystatin C and acute kidney injury after cardiopulmonary bypassClin J Am Soc Nephrol 2010; 5: 1373-9. [CrossRef] [PubMed] [PMC Free Article]

12. Heise D, Rentsch K, Braeuer A, Friedrich M, Quintel M, Comparison of urinary neutrophil glucosaminidase-associated lipocalin, cystatin C, and a1-microglobulin for early detection of acute renal injury after cardiac surgeryEur J Cardiothorac Surg 2011 39: 38-43. [CrossRef] [PubMed]

13. Nejat M, Pickering JW, Walker RJ, Westhuyzen J, Shaw GM, Frampton CM, Urinary cystatin C is diagnostic of acute kidney injury and sepsis, and predicts mortality in the intensive care unitCrit Care 2010; 14: R85. [CrossRef] [PubMed] [PMC Free Article]

14. Nejat M, Pickering JW, Walker RJ, Endre ZH, Rapid detection of acute kidney injury by plasma cystatin C in the intensive care unitNephrol Dial Transplant 2010; 25: 3283-9. [CrossRef] [PubMed]

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