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|Contrast-Media Induced Nephropathy and Diagnostic CT
- Predisposing factors for iodinated contrast media induced nephropathy (CIN) include chronic
renal insufficiency, diabetes, dehydration, congestive heart failure, nephrotoxic medications,
and age > 70 years
- For those with predisposing factors, an estimated glomerular filtration rate (eGFR) should be
calculated to stratify risk
- For those at highest risk, iodinated contrast agents should be avoided unless absolutely necessary
- For those at intermediate risk, prevention is recommended, including hydration and cessation
of nephrotoxic medications
media induced nephropathy (CIN) leading to acute renal failure is a
rare event associated with the exposure to iodinated contrast agents.
However, because of the increased utilization of procedures that use
iodinated contrast particularly diagnostic CT and catheter angiography,
CIN has become one of the leading causes of hospital-acquired acute
renal failure, accounting for 12% of all cases. While CIN is much more
common in hospitalized patients undergoing catheter angiography than in
outpatient contrast-enhanced CT examinations, identification of
patients at risk for developing CIN in both patient groups as well as
implementation of CIN prevention strategies is important for ensuring
high quality and safe patient care. In this article we provide a
practical approach to CIN prevention through risk stratification and
Predisposing Risk Factors
with the highest risk of developing CIN (Table 1) are those with
pre-existing renal insufficiency or chronic kidney disease. Other risk
factors include diabetes, dehydration, congestive heart failure,
advanced age, certain medications including prior iodinated contrast
administration (Figure 1). The combination of renal insufficiency and
diabetes is particularly problematic. However, in patients with
diabetes and no renal insufficiency, the risk of developing CIN seems
not to be increased. Multiple myeloma had been considered to be a risk
factor for CIN. However, it does not appear that this is a significant
risk factor when modern contrast agents are used, provided that
precautions are taken to ensure that these patients are adequately
hydrated and not significantly hypocalcemic. Finally, metformin has
been associated with post-contrast administration lactic acidosis and,
as a precautionary measure should be discontinued for all patients
undergoing a contrast enhanced CT scan and resumed after 48 hours.
The cornerstone of risk stratification is obtaining complete medical
history and, in patients with risk factors (Table 1), an estimate of
Figure 1. CT scan demonstrating contrast induced nephropathy
- A CT without contrast administration in a patient who had undergone a
contrast-enhanced CT scan followed by coronary catheter angiography
three days before demonstrates retention of iodinated contrast in the
renal cortices bilaterally (arrows). Serum creatinine values
increased from a baseline of 1.6 to 3.2 at the time of this CT exam.
|Table 1. Predisposing factors for the development of contrast-induced nephropathy with CT examination
|Coexisting medical/demographic factors:
- Renal insufficiency
- Congestive heart failure
- Age > 75 yrs
- Multiple myeloma
|Concurrent use of potentially nephrotoxic medications:
- Non-steroidal anti-inflammatory agents (NSAIDS)
- Cisplatin-based chemotherapy agents
- Aminoglycoside antibiotics
- Iodinated contrast within last 72 hours
high serum creatinine levels have traditionally been regarded as an
indicator of renal insufficiency, it is now recognized that creatinine
levels in isolation are a poor measure of renal function as they vary
with muscle mass Therefore, current recommendations are that the
estimated glomerular filtration rate (eGFR), as calculated using the
Modification of Diet in Renal Disease (MDRD) equation, be used to
determinate baseline renal function. The MDRD eGFR equation
requires inputs of serum creatinine, patient age, and race as follows:
GFR (mL/min/1.73 m2) = 186 x (Serum
Creatinine)-1.154 x (Age)-0.203 x (0.742 if female) x (1.210 if African American)
eGFR is now often provided along with serum creatinine by hospital chemistry laboratories. If unreported, eGFR calculators
can readily be found on the Internet, are available for personal
digital assistants, and as handheld plastic quick reference pocket
Thus, prior to a patient undergoing
contrast-enhanced CT study, a comprehensive medical history must be
obtained to identify any predisposing factors for CIN (Figure 2).
Patients with risk factors will require a serum creatinine level to
calculate the eGFR prior to the study.
|Figure 2. Guidelines for risk stratification and prophylaxis for CIN
Estimated GFR < 30 mL/min/1.73 m2
|Estimated GFR 30-60
|Estimated GFR > 60
||Encouraged, starting on day prior to examination
||Encouraged, starting on day prior to examination
Normal (0.9%) saline infused at 1 mL/kg for 24 hours starting 12 hours
prior to contrast exposure (Half-normal saline (0.45%) if patient has
evidence of CHF)
IV Bolus hydration (250 cc before and after study)
|N-Acetylcysteine (Mucomyst)† (Optional)
||600mg PO BID starting on day prior and for 48 hours after study
medications at least 48 hours prior; resume 48 hours after if
no evidence of CIN
||Obtain follow-up serum creatinine in 24 - 48 hours
If contrast administration is required in high-risk patients, direct
discussion with a radiologist and clinical nephrology service is
recommended for a patient-specific imaging and prophylaxis strategy.
†N-acetyl cysteine is an optional prophylactic measure for CIN as no convincing evidence of efficacy is available.
those at highest risk for developing CIN, contrast should be avoided
and alternate diagnostic examinations should be considered.
For all patients with low risk (eGFR > 60 ml / min / 1.73m2) and intermediate risk (eGFR between 30 and 60 ml/min/1.73m2), the following prophylactic measures can be taken to minimize the risk of CIN.
most important prophylactic measure is hydration. Prior to the day of
exam, all patients should be encouraged to have oral hydration.
Inpatients should receive intravenous normal (0.9%) saline infused at 1
mL/kg for 24 hours starting 12 hours prior to contrast exposure. For
patients in whom high salt load is a concern (e.g. advanced congestive
heart failure or kidney disease), half-normal (0.45%) saline may be
used. Outpatients should be reminded by the referring physician to
start hydration on the day prior to the imaging study. Bolus hydration
with 250cc before and after imaging study with normal saline is
typically administered in the MGH Department of Radiology.
Discontinuation of Nephrotoxic Medications. Nephrotoxic
medications, including NSAIDS, cisplatin-based agents, and
aminoglycoside, should be discontinued 48 hours before the test if
possible and not resumed until either 48 hours after or when renal
function is confirmed to have normalized after contrast administration.
It is also important to note that metformin, although not directly
nephrotoxic, should be discontinued at least one day prior to contrast
administration and not resumed until 48 hours after the imaging study.
Follow-up after Completion of CT Examination
For patients at intermediate to high risk for CIN, a follow-up
creatinine level and/or eGFR should be determined 24-48 hours after the
test as most cases will demonstrate changes in renal function within
that time period. If there is any evidence of CIN, a nephrologist
should be consulted for further management.
||MRI Contrast Agents in Renal Insufficiency Patients
In addition, it should be noted that a newly described disease,
Nephrogenic Systemic Fibrosis (NSF), has been linked with exposure to
gadolinium contrast in patients with moderate to severe kidney failure.
Although very rare, physicians should be aware of this possible
complication before considering MRI for patients with kidney disease.
More information on this is available on the PCOI website.
CT can be performed at Mass General Imaging in Waltham, Mass General
Imaging Chelsea, or the main MGH campus and can be ordered online via
the Radiology Order Entry (http://mghroe
) or by calling 4-XRAY (617-724-9729)
further questions on contrast induced nephropathy, please contact
Dr. Sanjay Saini, M.D.
, Vice-Chairman, MGH Department of Radiology
(617-726-8396) or Dr. G. Choy, M.D.
, MGH Radiology Resident.
We would like to thank Drs. Saini and Choy as well as Rahul Kakkar, MD,
PhD, BWH Medicine Housestaff, and Ajay Singh, M.D., Clinical Director,
Renal division, Brigham and Women’s Hospital for their advice and
assistance in the preparation of this article.
This article provided useful information about the appropriate use of imaging studies:
Note: clicking one of these options will close this window.
Pannu N, Wiebe N, Tonelli M. (2006) Prophylaxis strategies for contrast-induced
nephropathy. JAMA 295:2765-79.
Katzberg RW, Haller C. (2006) Contrast-induced nephrotoxicity: clinical landscape. Kidney Int Suppl 100:S3-7.
McCullough PA, Soman SS. (2005) Contrast-induced nephropathy. Crit Care Clin 21:261-80.
Elicker BM, Cypel YS, Weinreb JC. (2006) IV contrast administration for
CT: a survey of practices for the screening and prevention of contrast
nephropathy. AJR Am J Roentgenol 186:1651-8.
van den Berk G, Tonino S, de Fijter C, Smit W, Schultz MJ. (2005)
Bench-to-bedside review: preventive measures for contrast-induced
nephropathy in critically ill patients. Crit Care9:361-70.
Rudnick MR, Kesselheim A, Goldfarb S. (2006) Contrast-induced
nephropathy: How it develops, how to prevent it. Cleve Clin J Med