Journal of Clinical and Preventive Cardiology

: 2020  |  Volume : 9  |  Issue : 4  |  Page : 126--128

Contrast-Associated Acute Kidney Injury: Is It Contrast Nephrotoxicity Alone?

Dinesh Bansal, Vijay Kher 
 Division of Nephrology and Kidney Transplant Medicine, Medanta The Medicity, Gurugram, Haryana, India

Correspondence Address:
Dr. Vijay Kher
Department of Nephrology and Transplant Medicine, Medanta – The Medicity, Sector – 38, Gurgaon – Haryana – 122 001

How to cite this article:
Bansal D, Kher V. Contrast-Associated Acute Kidney Injury: Is It Contrast Nephrotoxicity Alone?.J Clin Prev Cardiol 2020;9:126-128

How to cite this URL:
Bansal D, Kher V. Contrast-Associated Acute Kidney Injury: Is It Contrast Nephrotoxicity Alone?. J Clin Prev Cardiol [serial online] 2020 [cited 2021 Mar 6 ];9:126-128
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Full Text

Contrast-enhanced studies are commonly used procedures in medical practice. As per the latest statistics of American heart association (AHA), more than a million cardiac catheterizations and 480,000 coronary angiograms are done yearly.[1] Adding to that computed tomography (CT) scan and other studies, the numbers are enormous. The number was 80 million contrast doses 10 years back. The numbers are likely to be many more today. Ever since Bartels et al. have reported anuria in a myeloma patient after intravenous pyelogram in 1954, contrast-associated acute kidney injury (CA-AKI) has been a matter of concern while ordering contrast studies.[2] CA-AKI has been defined by rise in creatinine by 0.3 mg/dL or 0.5 mg/dL 48–72 h after contrast use (AKIN or RIFLE criteria).[3],[4] Whether the contrast agent has a causal relationship to the development of AKI, is questionable in view of lack of control group (without contrast) in most of the studies.[5],[6],[7]

 Risk Factors for Contrast-Associated Acute Kidney Injury

Various factors have been looked upon regarding patient's risk of developing AKI after contrast exposure. Diabetes mellitus and renal insufficiency, type, dose, and route of administration have been considered risk factors for CA-AKI. A randomized trial by Rudnick showed that patients with serum creatinine >1.5 mg/dL have more than twenty times greater risk AKI than patients without renal insufficiency. Patients with diabetes mellitus had a 3.4 times greater risk for nephrotoxicity. This risk is maximum in patients who have diabetes as well as renal insufficiency. To avoid the effect of selection bias and other confounding factors, propensity score-matched studies have been done. Most of these studies have shown that patients with epidermal growth factor receptor <30 mL/min have greatest risk of CA-AKI.[8],[9],[10] However, all these risk factors are associated with AKI even without contrast and therefore controls without contrasts are necessary to confirm the causal association of contrast to AKI. Propensity-matched studies do show that the incidence of CA-AKI even if it occurs is not as high as reported in most studies in the past.[11]

High osmolar contrast media (CM) has higher risk of AKI as compared to low osmolar contrast media (LOCM) in the presence of baseline renal insufficiency. There was no significant difference between the type of contrast agent in patients without renal insufficiency. Iso-osmolar CM has no significant difference with respect to AKI as compared to LOCM. The dose of CM is a risk factor with higher volume of contrast media being associated with higher risk of AKI.[8],[12],[13]

Intra-arterial CM exposure has been shown to have higher risk of AKI as compared to intravenous route. However, whether it is due to higher nephrotoxicity of intra-arterial route or related to altered hemodynamics of acute myocardial infarction and comorbidities versus a diagnostic study like contrast CT scan is open to question.[14],[15],[16] Because AKI is associated with increased morbidity and all-cause mortality, fear of CA-AKI has handicapped the decision-making regarding contrast use.[17],[18] The studies of therapeutic interventions in patients with a high risk of CA-AKI have shown the volume expansion to be the only modality that has reduced the incidence of CA-AKI. Volume expansion has been attempted by various fluids – 0.45% saline and 0.9% saline isotonic bicarbonate fluids. 0.9% saline has been the fluid of choice and N-acetyl cysteine (NAC), fanoldapam, and mannitol have failed the scrutiny of scientific studies.[19],[20],[21],[22],[23]

The present study in this issue by Wani et al. is a noninterventional observational study, in which the investigators have tried to assess the risk factors associated with CA-AKI in patients undergoing percutaneous coronary interventions at a tertiary care center in India. This study, like other studies, finds that patients with diabetes, heart failure, and eGFR <60 mL/min have higher risk for CA-AKI.

Recent literature suggests that the risk of CA-AKI is overstated. CA-AKI in itself may not necessarily be the reflection of nephrotoxicity of CM, but is likely to be a result of a culmination of multiple factors. Acute illness mixed with the underlying comorbidities and risk factors result in AKI and CM may be just another risk factor, and assessing its true role in the causation of CA-AKI is not helped by the current literature.[6],[7]

In practice, a clinician should make the decision regarding contrast use based on overall patient management rather than the fear of CA-AKI. The impact of withholding contrast study for fear of CA-AKI and inability to provide effective therapeutic intervention needs to be weighed in every clinical situation. Although it will be prudent to expose the patient to CM when renal function is stable, the uniqueness of the clinical situation should be kept in mind. A timely coronary intervention may prove to be life-saving decision in a particular patient with chronic kidney disease or diabetes.

We strongly recommend increased discussion between the clinician and interventional radiologist/cardiologist on the added value of contrast enhancement to patient's clinical management. The new interventional techniques to minimize or zero contrast use should be encouraged.[24]


We conclude that the process of patient selection and careful evaluation of risk versus benefit in every patient who is to undergo a contrast study needs to be considered [Figure 1]. If desired information can be achieved by contrast ultrasound and magnetic resonance imaging with new gadolinum contrast, unnecessary risk of CA-AKI should be avoided. However, if contrast use will help in the patient diagnosis and management, then it should be used after volume expansion and minimizing the dose of contrast without any hesitation.{Figure 1}


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