ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Prevention of contrast-induced acute kidney injury associated with computed tomography

Prevention of contrast-induced acute kidney injury associated with computed tomography
Literature review current through: May 2024.
This topic last updated: Jan 09, 2024.

INTRODUCTION — Acute kidney injury (AKI) may develop after administration of iodinated contrast material [1-11]. AKI that is judged to be caused by iodinated contrast material (ie, after exclusion of other possible etiologies) has historically been called contrast-induced nephropathy (CIN) but has since been termed contrast-induced AKI (CI-AKI). AKI developing after contrast material administration is reversible in most cases, but its development may be associated with adverse outcomes [12]. (See "Contrast-associated and contrast-induced acute kidney injury: Clinical features, diagnosis, and management", section on 'Diagnosis'.)

This topic provides recommendations for the prevention of CI-AKI in patients expected to receive intravenous iodinated contrast material with computed tomography (CT) [13]. Other related topics describe:

Prevention of CI-AKI in patients expected to receive intra-arterial iodinated contrast material for angiography (see "Prevention of contrast-associated acute kidney injury related to angiography")

Diagnostic evaluation of patients in preparation for iodinated contrast material before referral for CT (see "Patient evaluation prior to oral or iodinated intravenous contrast for computed tomography")

TERMINOLOGY — Acute kidney injury (AKI) that occurs shortly after administration of iodinated contrast may or may not be causally related to contrast material:

"Post-contrast AKI" or "contrast-associated AKI" are broad terms that refer to AKI occurring shortly after administration of iodinated contrast and that may or may not be directly caused by the contrast material.

"Contrast-induced AKI (CI-AKI)," previously called "contrast-induced nephropathy (CIN)," is a specific term that refers to the subset of post-contrast AKI that is thought to be causally linked to contrast material administration (although a causal linkage cannot be established with certainty in epidemiologic studies).

Intravascular iodinated contrast media have been considered nephrotoxic based in large part upon animal experiments and uncontrolled human studies [14,15]. However, because many of these older reports lacked comparable control groups that did not receive contrast material, their applicability to our understanding of CI-AKI is unclear. Large controlled studies have since suggested that many cases of AKI following contrast administration may in fact be related to coincident nephrotoxic exposures (eg, hypovolemia, cardiac dysfunction, infection) present at the time that contrast material was administered [15-26].

As a result of these larger studies, multiple authorities in the radiology and nephrology communities adopted alternate terms ("post-contrast AKI" and "contrast-associated AKI") to refer to any AKI that occurs shortly after administration of iodinated contrast material [27]. Such terms are agnostic to cause and include both CI-AKI as well as coincidental AKI. Since coincident AKI is so common, true CI-AKI is difficult to diagnose accurately in the context of a clinical study and generally requires a study design with a control arm not exposed to contrast material [14-25,27]. Thus, the term "CI-AKI" (or "CIN") should be reserved for AKI that can be causally linked to contrast material administration, while the terms "post-contrast AKI" and "contrast-associated AKI" should be used to reflect any AKI that develops shortly after contrast material exposure.

EPIDEMIOLOGY — The reported incidence of post-contrast acute kidney injury (AKI), broadly, and contrast-induced AKI (CI-AKI), specifically, varies widely depending upon the definition, the presence or absence of risk factors, the type of contrast used, the volume of contrast material administered, the route of administration, and the patient population examined. In the absence of risk factors, the incidence of CI-AKI is negligible.

Incidence — Large, retrospective, cohort studies that included high-risk patients receiving iodinated contrast material with computed tomography (CT) as well as an appropriate, propensity-matched control group reported that the incidence of post-contrast AKI was high, ranging from 12 to 50 percent [17,18,28-31]. Conversely, the incidence of CI-AKI in these studies was, overall, negligible. Several of these cohorts found no risk of CI-AKI, regardless of baseline chronic kidney disease (CKD), although others identified CI-AKI in patients with severely reduced estimated glomerular filtration rate (eGFR), specifically among those with eGFR <30 mL/min/1.73 m2 [17,18,28-30]. Conclusions from these studies can be summarized as follows:

eGFR ≥45 mL/min/1.73 m2 – Among the general population of patients with eGFR ≥45 mL/min/1.73 m2, CI-AKI from intravenous iodinated contrast material administration generally does not occur.

eGFR of 30 to 44 mL/min/1.73 m2 – There may be a small risk of CI-AKI in patients with eGFR of 30 to 44 mL/min/1.73 m2, but the exact incidence in this population is uncertain. In one large propensity-matched study, for example, the incidence of AKI in patients with this degree of baseline kidney dysfunction was 1 percent higher among those undergoing a contrast-enhanced CT compared with those undergoing an unenhanced CT (16 versus 15 percent) [29].

eGFR <30 mL/min/1.73 m2 – The risk of CI-AKI in patients with eGFR <30 mL/min/1.73 m2 appears to be higher. In one large, propensity-matched study, post-contrast AKI developed in 35 percent of patients with baseline eGFR <30 mL/min/1.73 m2 who underwent contrast-enhanced CT and in 14 percent who underwent unenhanced CT [29].

Although these propensity-matched studies are the best available data to determine risk for AKI after intravenous contrast administration, they may be limited by the possibility of unmeasured confounders that could result in residual selection bias. An alternative explanation for the equivalent incidence of AKI among those receiving and not receiving iodinated contrast may be a higher risk of coincident AKI in control patients, which could obscure the contribution of contrast media to the AKI seen in contrast-exposed patients.

Risk factors — Factors that increase the risk of post-contrast AKI include [2,7,9,13,32-35]:

Impaired kidney function prior to contrast material administration – Impairment of kidney function, whether due to CKD or an ongoing episode of AKI, is the primary risk factor for post-contrast AKI. (See 'Identifying high-risk patients' below.)

Among patients with CKD, risk of post-contrast AKI is higher among those with lower baseline eGFR and may be potentiated by diabetes mellitus [4,32]. In one study, for example, the incidence of post-contrast AKI in patients whose baseline serum creatinine was >1.5 mg/dL (133 mmol/L) was 33 percent in diabetic patients and 12 percent in nondiabetic patients [4]. Diabetes was not associated with an increased risk among those with baseline serum creatinine <1.5 mg/dL. However, other studies, while supporting an association between reduced baseline kidney function and higher risk of post-contrast AKI, failed to identify diabetes as an additive risk factor, regardless of baseline eGFR [29].

Reduced kidney perfusion – Reduced kidney perfusion, which is often due to heart failure, hypovolemia, hemodynamic instability, or drugs that affect kidney hemodynamics, may be associated with a higher risk of post-contrast AKI. The association of these risk factors with post-contrast AKI has been observed in some, but not all, studies. The factors that reduce kidney perfusion may exacerbate the risk for post-contrast AKI or may be coincident to it [36].

Type of contrast material – Use of high-osmolality contrast media (HOCM) is associated with an increased risk of post-contrast AKI compared with use of low-osmolality contrast media (LOCM) or iso-osmolality contrast media (IOCM) [4,5,11,33,37]. However, HOCM is no longer used in modern clinical practice for intravascular administration and is therefore no longer an important risk factor for CI-AKI.

In general, when given intravenously, there is no clinically important difference in risk of post-contrast AKI comparing IOCM with LOCM. However, iohexol (a specific LOCM) may be associated with a greater risk of post-contrast AKI compared with other LOCM. (See "Prevention of contrast-associated acute kidney injury related to angiography".)

Other potential risk factors have been identified for post-contrast AKI after intra-arterial administration of contrast material; these include the volume of contrast material, proteinuria, hyperglycemia, and use of renin-angiotensin-aldosterone system inhibitors, such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs). Whether any of these are important risk factors for AKI after intravenous contrast administration is unclear. These potential risk factors are discussed elsewhere. (See "Prevention of contrast-associated acute kidney injury related to angiography".)

IDENTIFYING HIGH-RISK PATIENTS — The risk of contrast-induced acute kidney injury (CI-AKI) among patients referred for contrast-enhanced computed tomography (CT) primarily depends upon kidney function (algorithm 1) [4,6,9,11,13,32,33,38-40]. Patients with unknown kidney function should have an estimated glomerular filtration rate (eGFR) calculated if they have risk factors for kidney function impairment. The specific factors used to identify an at-risk patient and thereby justify kidney function screening vary depending upon how sensitive or specific a radiology practice wishes to be with respect to identifying high-risk patients [27]. Evaluation of a patient's kidney function in preparation for CT is described elsewhere. (See "Patient evaluation prior to oral or iodinated intravenous contrast for computed tomography", section on 'Assessing risk for contrast-induced acute kidney injury'.)

Clinically important nephrotoxicity due to intravenous iodinated contrast material is uncommon in patients undergoing CT who are not at high risk for this complication. Patients who should receive preventive measures are those who do not have contraindications for prophylaxis and who meet one of the following criteria (algorithm 1):

Stable eGFR <30 mL/min/1.73 m2 and not on dialysis.

Ongoing episode of AKI.

In addition, some (but not all) experts prescribe prophylaxis for select patients with stable eGFR 30 to 44 mL/min/1.73 m2 who are not on dialysis but who have multiple other potential risk factors. (See 'Risk factors' above.)

In general, patients with a stable eGFR ≥30 mL/min/1.73 m2, patients on dialysis, and patients who require an emergency CT to diagnose a life-threatening condition do not require preventive measures. (See "Patient evaluation prior to oral or iodinated intravenous contrast for computed tomography", section on 'Patients with impaired kidney function'.)

Occasionally, clinical care providers may choose to pursue prophylactic measures in patients with eGFR 30 to 44 mL/min/1.73 m2 who have multiple risk factors for post-contrast AKI (see 'Risk factors' above). Although observational studies failed to identify a significantly increased incidence of CI-AKI in this group of patients, the impact of multiple risk factors (eg, proteinuria, diabetes, heart failure) have not been well studied. Thus, it is possible that patients with multiple concomitant risk factors may be at risk of CI-AKI, even if the larger cohort is not. If there is uncertainty about the risks and benefits of performing an unenhanced or enhanced CT scan in a specific patient, the ordering provider can contact the radiologist to clarify. As with any procedure, a full discussion of the risks and benefits should be discussed with the patient by the ordering provider.

PREVENTION AMONG HIGH-RISK PATIENTS

Our approach — For patients at high risk for acute kidney injury (AKI) after intravenous contrast material administration with computed tomography (CT) (algorithm 1), we take the following approach (see 'Identifying high-risk patients' above):

Verify that iodinated contrast material is necessary. If an alternative test is likely to provide an accurate and reliable diagnosis, we proceed without administering contrast material. (See 'Verify that contrast material is necessary' below.)

Among euvolemic and hypovolemic inpatients, and emergency department patients whose clinical course permits it, we administer intravenous isotonic saline. Hypervolemic patients and patients receiving dialysis in general are not given volume expansion. There are no established dosing, duration, or injection rate recommendations for how the saline should be administered. Commonly used regimens are presented below. (See 'Inpatients and those in the emergency department' below.)

In high-risk outpatients, we prefer volume expansion with intravenous isotonic saline, if feasible, similar to our approach among inpatients. However, outpatients are sometimes given oral hydration [41]. There are no established dosing or timing recommendations for how the oral hydration should be administered. Some encourage patient-directed oral hydration before and after the scan (eg, total one to two liters). (See 'Outpatients' below.)

Use low- or iso-osmolar contrast agents. Use of these agents is standard for all diagnostic imaging examinations. (See "Prevention of contrast-associated acute kidney injury related to angiography", section on 'Dose and type of contrast agent'.)

If a patient at high risk for contrast-induced AKI (CI-AKI) is taking a metformin-containing medication, it should be discontinued for a minimum of 48 hours after the procedure and, if AKI develops, not reinstated until the kidney function has improved. In addition, metformin should generally be avoided in patients with estimated glomerular filtration rate (eGFR) <30 mL/min/1.73 m2. (See 'Withdrawal of metformin and nephrotoxic drugs in high-risk patients' below.)

If a patient is taking noncritical nephrotoxic medications, these should generally be withheld for 48 hours after administration of contrast material at the discretion of the ordering clinician and, if AKI develops, not resumed until the kidney function has improved.

For patients who are not at high risk for AKI after contrast-enhanced CT, we verify the need for contrast material; however, we do not prescribe prophylactic measures, do not withdraw nephrotoxic medications, and do not suspend metformin.

Verify that contrast material is necessary — The indications for contrast material administration should be reviewed for all patients, particularly those considered high risk for CI-AKI. Alternative tests might include, for example, noncontrast CT, ultrasound, or magnetic resonance imaging. Imaging alternatives for many common clinical scenarios are discussed in the relevant UpToDate topics or in the American College of Radiology (ACR) Appropriateness Criteria [42]. A discussion with a radiologist is likely to be helpful in high-risk patients.

Volume expansion — We generally prescribe volume expansion in patients who are at high risk for CI-AKI, unless they are hypervolemic or are receiving dialysis. Determining whether a patient is at high risk for CI-AKI after CT is presented above (algorithm 1). (See 'Identifying high-risk patients' above.)

In general, patients without known AKI and with eGFR ≥30 mL/min/1.73 m2 do not require prophylactic measures [43]. In some circumstances (ie, patients with multiple potential risk factors and eGFR 30 to 44 mL/min/1.73 m2), the ordering provider may elect to administer prophylaxis, although such an approach is based upon indirect data from populations receiving intra-arterial (rather than intravenous) contrast.

Intravenous volume administration is commonly used in high-risk patients (AKI or eGFR <30 mL/min/1.73 m2 and not receiving dialysis) who require contrast-enhanced CT despite an absence of adequately designed randomized trials demonstrating benefit and observational evidence that a benefit is lacking [44,45]. However, indirect evidence from several trials of such patients undergoing coronary angiography (rather than intravenous contrast administration) found a benefit from intravenous saline versus either oral hydration or no saline for the prevention of post-contrast AKI. (See "Prevention of contrast-associated acute kidney injury related to angiography".)

Three trials have enrolled patients with chronic kidney disease (CKD) who were undergoing intravenous contrast material administration (rather than intra-arterial contrast material) for CT. However, none included patients who had eGFR <30 mL/min/1.73 m2 or AKI, and none found evidence of benefit from prophylactic intravenous fluid administration [43,46]:

A single-center, randomized trial (A MAstricht Contrast-Induced Nephropathy Guidelines Study [AMACING]) found similar rates of post-contrast AKI (defined as a 25 percent or greater increase in plasma creatinine) among 660 patients with stage IIIa (eGFR 45 to 59 mL/min/1.73 m2) or stage IIIb (eGFR 30 to 45 mL/min/1.73 m2) CKD who were assigned to receive prophylactic intravenous isotonic saline or no intravenous fluids. Approximately one-half of the patients underwent procedures for which intravenous contrast material was given [43]. Prophylactic volume expansion did not reduce the incidence of AKI (2.7 versus 2.6 percent). Adverse events including heart failure, hyponatremia, and arrhythmia were more common in the group receiving intravenous fluid (5.5 versus 0 percent). However, this trial has some potentially important limitations [47]. These include a lower-than-expected incidence of post-contrast AKI (ie, 2.6 percent), which may have been due to the fact that no patients had an eGFR <30 mL/min/1.73 m2 and only one-third had an eGFR 30 to 44 mL/min/1.73 m2). In addition, 35 percent of the population had a postprocedure serum creatinine level obtained five or six days after contrast material exposure, and therefore some cases of post-contrast AKI may have been missed.

In another trial of 139 patients with mild to moderate CKD who were undergoing CT pulmonary angiography, no prophylaxis was compared with a 250 mL intravenous bolus of sodium bicarbonate [46]. The incidence of post-contrast AKI was similar in both groups (7 versus 9 percent). In a similar trial of 554 patients with mild to moderate CKD, post-contrast AKI occurred at similar rates among those receiving, and not receiving, a 250 mL intravenous bolus of sodium bicarbonate (2.7 versus 3.1 percent) [48].

Each of these trials were limited by the small number of events and the fact that enrolled patients were not at high risk for CI-AKI after CT. This is relevant because high-risk patients are the only patients for whom prophylaxis is indicated.

Inpatients and those in the emergency department — Among euvolemic and hypovolemic inpatients, and emergency department patients whose clinical course permits it, we administer intravenous isotonic saline. Hypervolemic patients and patients receiving dialysis in general are not given volume expansion. There are no established dosing, duration, or injection rate recommendations for how the saline should be administered. Some commonly used intravenous regimens for inpatients and emergency department patients include (time permitting):

3 mL/kg for one hour preprocedure, and 1.5 mL/kg/hour during and four to six hours postprocedure (total postprocedure volume at least 6 mL/kg)

1 mL/kg/hour for 6 to 12 hours preprocedure, and 1 mL/kg/hour during and 6 to 12 hours postprocedure

When intravenous volume expansion is indicated, we use isotonic saline rather than a sodium bicarbonate-based infusion [49]. Although several trials suggested equivalent or better outcomes with sodium bicarbonate [49-65], a large, high-quality, randomized trial of 5177 adults undergoing angiography found no benefit of bicarbonate compared with normal saline [49]. In addition, isotonic saline is commercially available and is less expensive than bicarbonate, and there is no risk of compounding errors [45].

Outpatients — In outpatients at high risk for CI-AKI, we prefer intravenous isotonic saline prophylaxis using a regimen that is similar to the options described for inpatients. (See 'Inpatients and those in the emergency department' above.)

However, some clinicians and practices prescribe oral hydration rather than intravenous volume expansion in such patients [41]. There are no established dosing or timing recommendations for oral hydration; some encourage patient-directed oral hydration before and after the scan (eg, total one to two liters).

Low- or iso-osmolality contrast — In general, only low-osmolality contrast media (LOCM) and iso-osmolality contrast media (IOCM) are used for modern intravascular administrations. High-osmolality contrast media (HOCM) is no longer used due to a higher side effect profile. The type of contrast material used for a CT is typically determined by the hospital or radiology department and is not selected by the referring provider. (See "Patient evaluation prior to oral or iodinated intravenous contrast for computed tomography", section on 'Types of contrast material'.)

Iodinated contrast media are either ionic or nonionic and of variable osmolality [10,66]. LOCM have an osmolality of approximately 600 mOsm/kg. IOCM have an osmolality of approximately 300 mOsm/kg.

The choice between LOCM and IOCM for contrast-enhanced CT does not appear to substantially affect the risk of post-contrast AKI. As an example, in one meta-analysis of six randomized trials, intravenous administration of iodixanol (IOCM) failed to reduce the rate of post-contrast AKI compared with LOCM (pooled relative risk 0.84, 95% CI 0.42-1.71) [67]. In addition, there was no benefit on the need for kidney replacement therapy, cardiovascular outcomes, or death. A separate meta-analysis reached generally similar conclusions [68], although one particular LOCM (iohexol) was associated with a higher risk compared with IOCM.

Our approach is broadly consistent with guidelines from the ACR, the American College of Cardiology/American Heart Association (ACC/AHA), and Kidney Disease: Improving Global Outcomes (KDIGO) committee [45,69,70].

Withdrawal of metformin and nephrotoxic drugs in high-risk patients — In patients deemed to be at high risk for CI-AKI who are taking metformin and who are to undergo CT with administration of iodinated contrast material, we agree with the 2018 ACR guidelines that the drug should be temporarily discontinued at the time of, or prior to, the study and should be withheld for at least 48 hours. (See 'Identifying high-risk patients' above.)

Metformin should not be resumed until the kidney function has been reassessed by the ordering provider and found to be acceptable. In addition, metformin should generally be avoided in patients with eGFR <30 mL/min/1.73 m2. (See "Metformin in the treatment of adults with type 2 diabetes mellitus", section on 'Contraindications'.)

We also agree with the 2018 ACR guidelines that, among patients who are not high risk, there is no need to discontinue metformin.

Our approach differs from the original metformin package inserts approved by the US Food and Drug Administration (FDA), which state that metformin should be withheld temporarily for all patients undergoing imaging using intravenous iodinated contrast media. The rationale was that, if AKI were to develop due to contrast media, an accumulation of metformin could occur and result in lactic acidosis. However, that risk is believed to be negligible for patients not at high risk. (See "Metformin in the treatment of adults with type 2 diabetes mellitus", section on 'Lactic acidosis'.)

Our approach also differs from the 2016 US FDA labeling that recommended discontinuation of metformin in patients with an eGFR between 30 and 60 mL/min/1.73 m2.

Patients taking metformin are not at higher risk than other patients for CI-AKI [70,71]. In addition, among patients who are not at high risk for CI-AKI after CT, metformin does not need to be discontinued either prior to or following contrast material administration, and there is no need to reassess the patient's kidney function following the test or procedure.

Contrast dose — A dose-toxicity relationship following intravenous administration has not been observed as it has been for cardiac angiography. Additionally, the dose-toxicity relationship observed following cardiac angiography is a correlative one; patients are not randomly assigned to get higher or lower doses in such studies, limiting conclusions about dose toxicity. As an example, patients necessitating higher contrast material volumes may have a higher risk for post-contrast AKI. Separating patient and disease factors from contrast material-related factors is therefore complicated.

The contrast material dose given for a particular CT examination should be based upon what is necessary to obtain a reliable diagnostic examination. The contrast material dose should not be lowered ad hoc in high-risk patients for fear of AKI; otherwise, there is a risk of a nondiagnostic scan in addition to any potential risk from the contrast material.

If multiple doses of contrast material are indicated, there is no specific cumulative dose threshold above which contrast material should be delayed or withheld. In high-risk patients, if multiple sequential administrations are needed, judgment should be exercised with respect to the timing of the examinations and the clinical need for a timely diagnosis.

Other preventive measures we do not use — A variety of other measures have been attempted to reduce the risk of post-contrast AKI. Generally speaking, these are unproven and not recommended. (See "Prevention of contrast-associated acute kidney injury related to angiography".)

Prophylactic hemofiltration and hemodialysis — Prophylactic hemofiltration and hemodialysis are not indicated for the prevention of post-contrast AKI or CI-AKI. A 2012 meta-analysis that included eight studies of hemodialysis and three studies of hemofiltration/hemodiafiltration showed no benefit from these modalities on the incidence of post-contrast AKI [72].

In addition, prophylactic dialysis is not indicated for the prevention of volume overload or osmotic-induced electrolyte shifts from intravascular contrast material administration in most dialysis-dependent patients [73,74]. Similarly, there is no need for immediate dialysis after contrast material administration in order to preserve residual kidney function or to limit the risk of allergic-like reaction in hemodialysis patients [73,75-77]. Dialysis can typically wait until the next scheduled dialysis treatment.

Guided fluid repletion — Volume expansion strategies are listed above. (See 'Volume expansion' above.)

More invasive or elaborate means, such as measuring left ventricular end-diastolic pressure or use of the RenalGuard system (which replaces diuretic-induced urine output in real time with infusion of isotonic saline) are not indicated for the prevention of post-contrast AKI or CI-AKI related to intravenous administration.

Other measures — Other measures that lack evidence of efficacy to prevent post-contrast AKI in patients undergoing CT, and that we do not use, include acetylcysteine, remote ischemic preconditioning, withholding angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), statins, diuretics, oral sodium citrate, atrial natriuretic peptide, ascorbic acid, trimetazidine, and inhibitors of vasoconstriction (eg, fenoldopam).

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Chronic kidney disease in adults".)

SUMMARY AND RECOMMENDATIONS

Definitions – Acute kidney injury (AKI) that occurs shortly after administration of iodinated contrast material may or may not be causally related to the contrast material:

"Post-contrast AKI" or "contrast-associated AKI" are broad terms that refer to AKI occurring shortly after administration of iodinated contrast and that may or may not be directly caused by the contrast material.

"Contrast-induced AKI (CI-AKI)," previously called "contrast-induced nephropathy (CIN)," is a specific term that refers to the subset of post-contrast AKI that can be causally linked to contrast material administration.

Epidemiology – The reported incidence of post-contrast AKI, broadly, and CI-AKI, specifically, varies widely depending upon the definition, the presence or absence of risk factors, the volume of contrast material administered, the route of administration, and the patient population examined. In the absence of risk factors, the incidence of CI-AKI is negligible. The primary risk factor is impairment of kidney function, whether due to chronic kidney disease (CKD) or an ongoing episode of AKI. Other potential risk factors may include diabetes mellitus, factors that reduce kidney perfusion (eg, heart failure, hypovolemia), proteinuria, and intra-arterial (rather than intravenous) contrast material administration. (See 'Epidemiology' above.)

Risk stratification – The risk of CI-AKI among patients referred for computed tomography (CT) primarily depends upon kidney function (algorithm 1) [4,6,9,11,32,33,39]. Patients who should receive preventive measures are those who do not have contraindications for prophylaxis and who meet one of the following criteria (see 'Identifying high-risk patients' above):

Stable estimated glomerular filtration rate (eGFR) <30 mL/min/1.73 m2 and not on dialysis.

Ongoing episode of AKI.

In addition, some (but not all) experts prescribe prophylaxis for select patients with stable eGFR 30 to 44 mL/min/1.73 m2 who are not on dialysis but who have multiple other potential risk factors. (See 'Risk factors' above.)

Management of high-risk patients – For patients at high risk for AKI after intravenous contrast material administration with CT (algorithm 1), we take the following approach (see 'Identifying high-risk patients' above):

Verify that iodinated contrast material is necessary. If an alternative test is likely to provide an accurate and reliable diagnosis, we proceed without administering contrast material. (See 'Verify that contrast material is necessary' above.)

Among euvolemic and hypovolemic inpatients, and emergency department patients whose clinical course permits it, we suggest intravenous isotonic saline rather than oral hydration or no intravenous fluid administration (Grade 2C). Hypervolemic patients and patients receiving dialysis in general are not given volume expansion. (See 'Inpatients and those in the emergency department' above.)

Among outpatients at high risk for CI-AKI, we suggest intravenous fluid administration rather than no fluid administration (Grade 2C). Oral hydration is an alternative that is used by some clinicians. (See 'Outpatients' above.)

Use low- or iso-osmolar contrast agents. Use of these agents is standard for intravascular administrations. (See "Prevention of contrast-associated acute kidney injury related to angiography", section on 'Dose and type of contrast agent'.)

If a high-risk patient is taking a metformin-containing medication, it should be discontinued for a minimum of 48 hours after the procedure and, if AKI develops, not reinstated until the kidney function has improved. If a patient is taking noncritical nephrotoxic medications, these should generally be withheld at the discretion of the ordering provider for 48 hours after administration of contrast material and, if AKI develops, not resumed until the kidney function has improved. (See 'Withdrawal of metformin and nephrotoxic drugs in high-risk patients' above.)

Interventions not recommended – A variety of other measures have been attempted to reduce the risk of post-contrast AKI. Generally speaking, these are unproven and not recommended. These include prophylactic hemofiltration and hemodialysis, guided fluid repletion, acetylcysteine, remote ischemic preconditioning withholding angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), statins, diuretics, oral sodium citrate, atrial natriuretic peptide, ascorbic acid, trimetazidine, and inhibitors of vasoconstriction (eg, fenoldopam). (See "Prevention of contrast-associated acute kidney injury related to angiography".)

  1. Rudnick MR, Berns JS, Cohen RM, Goldfarb S. Nephrotoxic risks of renal angiography: contrast media-associated nephrotoxicity and atheroembolism--a critical review. Am J Kidney Dis 1994; 24:713.
  2. Barrett BJ. Contrast nephrotoxicity. J Am Soc Nephrol 1994; 5:125.
  3. Asif A, Epstein M. Prevention of radiocontrast-induced nephropathy. Am J Kidney Dis 2004; 44:12.
  4. 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.
  5. Cigarroa RG, Lange RA, Williams RH, Hillis LD. Dosing of contrast material to prevent contrast nephropathy in patients with renal disease. Am J Med 1989; 86:649.
  6. Manske CL, Sprafka JM, Strony JT, Wang Y. Contrast nephropathy in azotemic diabetic patients undergoing coronary angiography. Am J Med 1990; 89:615.
  7. 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.
  8. 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.
  9. Rihal CS, Textor SC, Grill DE, et al. Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention. Circulation 2002; 105:2259.
  10. 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.
  11. Schwab SJ, Hlatky MA, Pieper KS, et al. Contrast nephrotoxicity: a randomized controlled trial of a nonionic and an ionic radiographic contrast agent. N Engl J Med 1989; 320:149.
  12. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol 2008; 3:263.
  13. Davenport MS, Perazella MA, Yee J, et al. Use of Intravenous Iodinated Contrast Media in Patients with Kidney Disease: Consensus Statements from the American College of Radiology and the National Kidney Foundation. Radiology 2020; 294:660.
  14. Davenport MS, Cohan RH, Khalatbari S, Ellis JH. The challenges in assessing contrast-induced nephropathy: where are we now? AJR Am J Roentgenol 2014; 202:784.
  15. Rao QA, Newhouse JH. Risk of nephropathy after intravenous administration of contrast material: a critical literature analysis. Radiology 2006; 239:392.
  16. Davenport MS, Khalatbari S, Dillman JR, et al. Contrast material-induced nephrotoxicity and intravenous low-osmolality iodinated contrast material. Radiology 2013; 267:94.
  17. McDonald RJ, McDonald JS, Bida JP, et al. Intravenous contrast material-induced nephropathy: causal or coincident phenomenon? Radiology 2013; 267:106.
  18. Davenport MS, Khalatbari S, Cohan RH, et al. Contrast material-induced nephrotoxicity and intravenous low-osmolality iodinated contrast material: risk stratification by using estimated glomerular filtration rate. Radiology 2013; 268:719.
  19. McDonald JS, McDonald RJ, Carter RE, et al. Risk of intravenous contrast material-mediated acute kidney injury: a propensity score-matched study stratified by baseline-estimated glomerular filtration rate. Radiology 2014; 271:65.
  20. McDonald JS, McDonald RJ, Comin J, et al. Frequency of acute kidney injury following intravenous contrast medium administration: a systematic review and meta-analysis. Radiology 2013; 267:119.
  21. Katzberg RW, Newhouse JH. Intravenous contrast medium-induced nephrotoxicity: is the medical risk really as great as we have come to believe? Radiology 2010; 256:21.
  22. Newhouse JH, Kho D, Rao QA, Starren J. 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.
  23. Katzberg RW, Barrett BJ. Risk of iodinated contrast material--induced nephropathy with intravenous administration. Radiology 2007; 243:622.
  24. Hinson JS, Ehmann MR, Fine DM, et al. Risk of Acute Kidney Injury After Intravenous Contrast Media Administration. Ann Emerg Med 2017; 69:577.
  25. McDonald JS, McDonald RJ, Williamson EE, et al. Post-contrast acute kidney injury in intensive care unit patients: a propensity score-adjusted study. Intensive Care Med 2017; 43:774.
  26. Wilhelm-Leen E, Montez-Rath ME, Chertow G. Estimating the Risk of Radiocontrast-Associated Nephropathy. J Am Soc Nephrol 2017; 28:653.
  27. American College of Radiology. Committee on Drugs and Contrast Media. ACR Manual on Contrast Media, Version 10.3. 2017. 2017. https://www.acr.org/Quality-Safety/Resources/Contrast-Manual (Accessed on July 10, 2017).
  28. Davenport MS, Cohan RH, Ellis JH. Contrast media controversies in 2015: imaging patients with renal impairment or risk of contrast reaction. AJR Am J Roentgenol 2015; 204:1174.
  29. Ellis JH, Khalatbari S, Yosef M, et al. Influence of Clinical Factors on Risk of Contrast-Induced Nephrotoxicity From IV Iodinated Low-Osmolality Contrast Material in Patients With a Low Estimated Glomerular Filtration Rate. AJR Am J Roentgenol 2019; 213:W188.
  30. Dekkers IA, van der Molen AJ. Propensity Score Matching as a Substitute for Randomized Controlled Trials on Acute Kidney Injury After Contrast Media Administration: A Systematic Review. AJR Am J Roentgenol 2018; 211:822.
  31. Rudnick MR, Leonberg-Yoo AK, Litt HI, et al. The Controversy of Contrast-Induced Nephropathy With Intravenous Contrast: What Is the Risk? Am J Kidney Dis 2020; 75:105.
  32. Parfrey PS, Griffiths SM, Barrett BJ, et al. Contrast material-induced renal failure in patients with diabetes mellitus, renal insufficiency, or both. A prospective controlled study. N Engl J Med 1989; 320:143.
  33. Lautin EM, Freeman NJ, Schoenfeld AH, et al. Radiocontrast-associated renal dysfunction: incidence and risk factors. AJR Am J Roentgenol 1991; 157:49.
  34. Nikolsky E, Mehran R, Lasic Z, et al. Low hematocrit predicts contrast-induced nephropathy after percutaneous coronary interventions. Kidney Int 2005; 67:706.
  35. 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.
  36. Wang K, Li HL, Bei WJ, et al. Association of left ventricular ejection fraction with contrast-induced nephropathy and mortality following coronary angiography or intervention in patients with heart failure. Ther Clin Risk Manag 2017; 13:887.
  37. 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.
  38. Obed M, Gabriel MM, Dumann E, et al. Risk of acute kidney injury after contrast-enhanced computerized tomography: a systematic review and meta-analysis of 21 propensity score-matched cohort studies. Eur Radiol 2022; 32:8432.
  39. Barrett BJ, Parfrey PS, Vavasour HM, et al. Contrast nephropathy in patients with impaired renal function: high versus low osmolar media. Kidney Int 1992; 41:1274.
  40. Goulden R, Rowe BH, Abrahamowicz M, et al. Association of Intravenous Radiocontrast With Kidney Function: A Regression Discontinuity Analysis. JAMA Intern Med 2021; 181:767.
  41. Sebastià C, Páez-Carpio A, Guillen E, et al. Oral hydration as a safe prophylactic measure to prevent post-contrast acute kidney injury in oncologic patients with chronic kidney disease (IIIb) referred for contrast-enhanced computed tomography: subanalysis of the oncological group of the NICIR study. Support Care Cancer 2022; 30:1879.
  42. American College of Radiology. ACR Appropriateness Criteria. https://acsearch.acr.org/list (Accessed on February 12, 2019).
  43. Nijssen EC, Rennenberg RJ, Nelemans PJ, et al. Prophylactic hydration to protect renal function from intravascular iodinated contrast material in patients at high risk of contrast-induced nephropathy (AMACING): a prospective, randomised, phase 3, controlled, open-label, non-inferiority trial. Lancet 2017; 389:1312.
  44. Yan P, Duan SB, Luo XQ, et al. Effects of intravenous hydration in preventing post-contrast acute kidney injury in patients with eGFR < 30 mL/min/1.73 m2. Eur Radiol 2023; 33:9434.
  45. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl 2012; 2:8.
  46. Kooiman J, Sijpkens YW, van Buren M, et al. Randomised trial of no hydration vs. sodium bicarbonate hydration in patients with chronic kidney disease undergoing acute computed tomography-pulmonary angiography. J Thromb Haemost 2014; 12:1658.
  47. Solomon R. Hydration to prevent acute kidney injury after angiography: the AMACING trial. Coron Artery Dis 2017; 28:629.
  48. Timal RJ, Kooiman J, Sijpkens YWJ, et al. Effect of No Prehydration vs Sodium Bicarbonate Prehydration Prior to Contrast-Enhanced Computed Tomography in the Prevention of Postcontrast Acute Kidney Injury in Adults With Chronic Kidney Disease: The Kompas Randomized Clinical Trial. JAMA Intern Med 2020; 180:533.
  49. Weisbord SD, Gallagher M, Jneid H, et al. Outcomes after Angiography with Sodium Bicarbonate and Acetylcysteine. N Engl J Med 2018; 378:603.
  50. Merten GJ, Burgess WP, Gray LV, et al. Prevention of contrast-induced nephropathy with sodium bicarbonate: a randomized controlled trial. JAMA 2004; 291:2328.
  51. 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.
  52. Recio-Mayoral A, Chaparro M, Prado B, et al. The reno-protective effect of hydration with sodium bicarbonate plus N-acetylcysteine in patients undergoing emergency percutaneous coronary intervention: the RENO Study. J Am Coll Cardiol 2007; 49:1283.
  53. Ozcan EE, Guneri S, Akdeniz B, et al. Sodium bicarbonate, N-acetylcysteine, and saline for prevention of radiocontrast-induced nephropathy. A comparison of 3 regimens for protecting contrast-induced nephropathy in patients undergoing coronary procedures. A single-center prospective controlled trial. Am Heart J 2007; 154:539.
  54. Hoste EA, De Waele JJ, Gevaert SA, et al. Sodium bicarbonate for prevention of contrast-induced acute kidney injury: a systematic review and meta-analysis. Nephrol Dial Transplant 2010; 25:747.
  55. 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.
  56. Maioli M, Toso A, Leoncini M, et al. Sodium bicarbonate versus saline for the prevention of contrast-induced nephropathy in patients with renal dysfunction undergoing coronary angiography or intervention. J Am Coll Cardiol 2008; 52:599.
  57. Alonso A, Lau J, Jaber BL, et al. Prevention of radiocontrast nephropathy with N-acetylcysteine in patients with chronic kidney disease: a meta-analysis of randomized, controlled trials. Am J Kidney Dis 2004; 43:1.
  58. Vasheghani-Farahani A, Sadigh G, Kassaian SE, et al. Sodium bicarbonate plus isotonic saline versus saline for prevention of contrast-induced nephropathy in patients undergoing coronary angiography: a randomized controlled trial. Am J Kidney Dis 2009; 54:610.
  59. Brar SS, Hiremath S, Dangas G, et al. Sodium bicarbonate for the prevention of contrast induced-acute kidney injury: a systematic review and meta-analysis. Clin J Am Soc Nephrol 2009; 4:1584.
  60. Solomon R, Gordon P, Manoukian SV, et al. Randomized Trial of Bicarbonate or Saline Study for the Prevention of Contrast-Induced Nephropathy in Patients with CKD. Clin J Am Soc Nephrol 2015; 10:1519.
  61. Joannidis M, Schmid M, Wiedermann CJ. Prevention of contrast media-induced nephropathy by isotonic sodium bicarbonate: a meta-analysis. Wien Klin Wochenschr 2008; 120:742.
  62. Zoungas S, Ninomiya T, Huxley R, et al. Systematic review: sodium bicarbonate treatment regimens for the prevention of contrast-induced nephropathy. Ann Intern Med 2009; 151:631.
  63. Klima T, Christ A, Marana I, et al. Sodium chloride vs. sodium bicarbonate for the prevention of contrast medium-induced nephropathy: a randomized controlled trial. Eur Heart J 2012; 33:2071.
  64. Subramaniam RM, Suarez-Cuervo C, Wilson RF, et al. Effectiveness of Prevention Strategies for Contrast-Induced Nephropathy: A Systematic Review and Meta-analysis. Ann Intern Med 2016; 164:406.
  65. Navaneethan SD, Singh S, Appasamy S, et al. Sodium bicarbonate therapy for prevention of contrast-induced nephropathy: a systematic review and meta-analysis. Am J Kidney Dis 2009; 53:617.
  66. Moore RD, Steinberg EP, Powe NR, et al. Nephrotoxicity of high-osmolality versus low-osmolality contrast media: randomized clinical trial. Radiology 1992; 182:649.
  67. Eng J, Wilson RF, Subramaniam RM, et al. Comparative Effect of Contrast Media Type on the Incidence of Contrast-Induced Nephropathy: A Systematic Review and Meta-analysis. Ann Intern Med 2016; 164:417.
  68. Heinrich MC, Häberle L, Müller V, et al. Nephrotoxicity of iso-osmolar iodixanol compared with nonionic low-osmolar contrast media: meta-analysis of randomized controlled trials. Radiology 2009; 250:68.
  69. Kushner FG, Hand M, Smith SC Jr, et al. 2009 focused updates: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction (updating the 2004 guideline and 2007 focused update) and ACC/AHA/SCAI guidelines on percutaneous coronary intervention (updating the 2005 guideline and 2007 focused update) a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2009; 54:2205.
  70. ACR Manual on Contrast Media. Version 10.3, American College of Radiology 2017. https://www.acr.org/-/media/ACR/Files/Clinical-Resources/Contrast_Media.pdf (Accessed on February 13, 2018).
  71. Kao TW, Lee KH, Chan WP, et al. Continuous use of metformin in patients receiving contrast medium: what is the evidence? A systematic review and meta-analysis. Eur Radiol 2022; 32:3045.
  72. Cruz DN, Goh CY, Marenzi G, et al. Renal replacement therapies for prevention of radiocontrast-induced nephropathy: a systematic review. Am J Med 2012; 125:66.
  73. Hamani A, Petitclerc T, Jacobs C, Deray G. Is dialysis indicated immediately after administration of iodinated contrast agents in patients on haemodialysis? Nephrol Dial Transplant 1998; 13:1051.
  74. Younathan CM, Kaude JV, Cook MD, et al. Dialysis is not indicated immediately after administration of nonionic contrast agents in patients with end-stage renal disease treated by maintenance dialysis. AJR Am J Roentgenol 1994; 163:969.
  75. Bahrainwala JZ, Leonberg-Yoo AK, Rudnick MR. Use of Radiocontrast Agents in CKD and ESRD. Semin Dial 2017; 30:290.
  76. Rodby RA. Preventing complications of radiographic contrast media: is there a role for dialysis? Semin Dial 2007; 20:19.
  77. Takebayashi S, Hidai H, Chiba T. No need for immediate dialysis after administration of low-osmolarity contrast medium in patients undergoing hemodialysis. Am J Kidney Dis 2000; 36:226.
Topic 112897 Version 10.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟