Elsevier

Current Problems in Diagnostic Radiology

Volume 44, Issue 6, November–December 2015, Pages 501-504
Current Problems in Diagnostic Radiology

Contrast-Induced Nephropathy: Identifying the Risks, Choosing the Right Agent, and Reviewing Effective Prevention and Management Methods,☆☆

https://doi.org/10.1067/j.cpradiol.2015.04.002Get rights and content

With the rise in the use of intravenous iodinated contrast media for both computed tomography scan and angiographic studies, there is a greater likelihood of complications. One of the most well-known adverse effects is contrast-induced media nephropathy, which is also called contrast-induced acute kidney injury. This is third most common cause of hospital acquired acute renal failure. It is associated with an increase in morbidity, mortality, and greater financial burden on healthcare system. Because of these factors, it is important for the radiologist to not only recognize risk factors, as well as the signs and symptoms, but also to know how to manage patients appropriately.

Introduction

The administration of intravenous iodinated contrast media has been of great value to the practice of radiology, but it is not without risks. One of the major risks is contrast-induced nephropathy (CIN). CIN has been associated with an increase in morbidity, mortality, as well as prolonged hospital course. It is believed to account for nearly 10% of hospital acquired acute renal failure.1, 2, 3 In addition, CIN is responsible for one in 6 patients, who are in the intensive care units because of decreased renal function, and on hemodialysis after intravenous (IV) contrast administration.4 This article will discuss the risk factors, recommend prophylactic measures, and discuss the management of such adverse event. In addition, this article will discuss some of the recent and more controversial topics regarding contrast-induced nephropathy.

Section snippets

Definition of CIN

CIN is defined as an absolute (>0.5 mg/dL) or relative (25%) increase in serum creatinine (SCr) within 48-72 hours after iodinated contrast medium administration in the absence of any other explanation for the rise in SCr.2 SCr will usually peak at 2-3 days following contrast media use and then returns slowly to baseline within 14 days. Yet, some patients progress quickly to acute renal failure, which may require hemodialysis.5, 6

The definition of acute renal failure is defined as the increase

Incidence

In patients without history of renal disease, the risk of CIN is less than 1%.9 It was previously believed that patients without any history of pre-existing renal insufficiency have 12%-27% of CIN, and if there was history of diabetic nephropathy, the incidence increases to 50%.10

Recent Controversies Regarding CIN

However, a recent study of over 50,000 patients undergoing over 150,000 scans by McDonald et al,11 which was published in Radiology in 2013, demonstrated that the risk of CIN with intravenous contrast has been overestimated if not exaggerated when adjusted for presumed risk factors when comparing patients who received IV contrast vs those who did not receive contrast. In another study by McDonald et al,12 who performed a meta-analysis and systemic review of over 1400 studies, found that the

Risk Factors

The single most important predictor of CIN risk is chronic kidney disease (CKD). Patients with CKD have an increased risk by more than 20 times that of a normal individual to develop CIN.16 Also, patients with a glomerular filtration rate (GFR) <30 mL/min at the time of contrast administration are also at the highest risk.17 In addition, pre-existing condition of renal insufficiency (SCr level > 1.5 mg/dL), diabetes mellitus, sepsis, hypotension, dehydration, cardiovascular disease, use of

Pathogenesis

Although the mechanism of CIN is not completely understood, it is hypothesized that the constriction of the vessels within the renal medulla leading to a reduction in oxygen delivery resulting in a direct toxic effect upon the tubular cells in the kidneys. Subsequently, the reduction in the perfusion in the kidney causes the activation of the tubule-glomerular feedback response and the release of endogenous vasoactive mediators such as endothelin and adenosine. This is followed by a reduction

Guidelines for the Prevention of CIN

Patients with a GFR > 60 mL/min have normal or near normal renal function and have very low risk of CIN and require no prophylaxis or follow-up.6

With a GFR <45-59 mL/min, there is a low risk of CIN in patients without risk factors. No specific prophylaxis or follow-up is required. For patients with receive intra-arterial contrast media preventative measures are recommended.

If the GFR is <45 mL/min, patients are at moderate risk for CIN and preventative measures are recommended. IV hydration is

Fluid Hydration

Intravenous therapy is the most reliable means to monitor and administer fluids. Fluid administration is the most important means of prevention. With regards to the type of fluid, isotonic sodium chloride is more protective than hypotonic saline and more effective volume expander.22

The protective effects of intravenous fluids work in 2 ways against CIN by primarily volume expansion of the intravascular space, thus decreasing the vasoconstrictive effects of contrast in the medulla by blocking

Metformin

Metformin is for patients with noninsulin-dependent diabetes mellitus whose hyperglycemia is not controlled by diet or sulfonylurea therapy alone. The mechanism of action is by decreasing hepatic glucose production, thus enhancing the peripheral glucose uptake in order to increase the sensitivity of peripheral tissues to insulin. Metformin is typically excreted in the kidneys by glomerular filtration and excretion. The most significant side effect is the potential of metformin associated lactic

Conclusion

The use of contrast adds great value for both computed tomography and angiographic studies. However, it is not with inherent risk factors. One of the most concerning risk factors is CIN. Therefore, it is important for the practicing radiologist to become familiar with the predisposing risks, the preventive measures, and recommendations for patients with special circumstances. With this information, patients will have better outcomes and have less of a likelihood of developing acute renal

References (40)

  • C. Briguori et al.

    Contrast agent–associated nephrotoxicity

    Prog Cardiovasc Dis

    (2003)
  • M.A. Stevens et al.

    A prospective randomized trial of prevention measures in patients at high risk for contrast nephropathy: Results of the P.R.I.N.C.E. Study

    J Am Coll Cardiol

    (1999)
  • P.A. McCullough et al.

    Contrast-induced nephropathy

    Crit Care Clin

    (2005)
  • A. Vasheghani-Farahani et al.

    Sodium bicarbonate plus isotonic saline versus saline for prevention of contrast-induced nephropathy in patients undergoing coronary angiography: A randomized controlled trial

    American J Kidney Dis

    (2009)
  • E.A. Hoste et al.

    Epidemiology of contrast-associated acute kidney injury in ICU patients: A retrospective cohort analysis

    Intensive Care Med

    (2011)
  • N. Pannu et al.

    Prophylaxis strategies for contrast-induced nephropathy

    J Am Med Assoc

    (2006)
  • S. Dirkes

    Acute kidney injury: Not just acute renal failure anymore?

    Crit Care Nurse

    (2011)
  • H.S. Thomsen et al.

    Adverse effects of contrast media: Incidence, prevention and management

    Drug Saf

    (1998)
  • S.K. Morcos et al.

    Adverse reactions to iodinated contrast media

    Eur Radiol

    (2001)
  • R.J. McDonald et al.

    Intravenous contrast material-induced nephropathy: Causal or coincident phenomenon?

    Radiology

    (2013)
  • Cited by (0)

    Presented as Education Exhibit, 100th RSNA meeting, Chicago, IL.

    ☆☆

    Disclosures: H.H.A. is supported by a research grant from Bracco Group. He is a consultant for the RGG Healthcare and also a consulting author for the Oxford University Press.

    View full text