Contrast-induced acute kidney injury (CI-AKI) following intra-arterial administration of iodinated contrast media (original) (raw)
Related papers
Journal of Vascular and Interventional Radiology, 2011
We report the incidence of contrast-induced acute kidney injury (CI-AKI) following administration of iodixanol or low-osmolar contrast media (LOCM) in patients for suspected peripheral arterial occlusive disease (PAOD) undergoing intra-arterial digital angiography (IA-DSA). Methods: IA-DSA was performed according to site standard for contrast agent type and volume following computed tomography (CT) of the abdominal aortoiliac and lower extremity arteries and a washout period of at least 3 days. Serum creatinine was measured at baseline and 24 ± 4 hours after contrast administration. CI-AKI was defined as laboratory increase of serum creatinine value ≥25% from baseline measurement at 24 hours. The incidence of CI-AKI was analyzed with chi-square statistics. Results: Of the 250 patients who underwent IA-DSA with complete data for analysis, 147 (58.8%) received iodixanol and 103 (41.2%) received LOCM (iopamidol, 91; ioversol, 7; iohexol, 3; iopromide, 2). Baseline mean serum creatinine was statistically higher for iodixanol compared with LOCM (100 vs. 82.7 µmol/L; p=0.0124). CI-AKI occurred in 8 patients (5.4%) with iodixanol and 14 patients (13.6%) with LOCM (p=0.025). Further analysis showed that iopamidol administration was responsible for the 13 out of 14 cases of CI-AKI in LOCM patients. Conclusions: In patients with suspected PAOD undergoing IA-DSA, the incidence of CI-AKI at 24 hours following contrast administration was significantly less for patients who received iodixanol compared with various LOCM; this difference was primarily driven by iopamidol.
American Heart Journal, 2013
Background Direct comparisons between risk of contrast induced acute kidney injury (CI-AKI) after intra-arterial versus intravenous contrast administration are scarce. We estimated and compared the risk of CI-AKI and its clinical course after both modes of contrast administration in patients who underwent both. Methods One hundred seventy patients who received both intra-arterial and intravenous contrast injections within one year between 2001 and 2010 were included. Primary outcome was occurrence of CI-AKI. Secondary outcomes were duration of hospital stay, the need for dialysis, recovery of renal function, and mortality. Results The risk of CI-AKI was 24/170 (14.0%, 95% CI 9.6-20.2) after intra-arterial contrast injection versus 20/170 (11.7%, 95% CI 7.7-17.5) after intravenous contrast administration, which led to a relative risk of 1.2 (95% CI 0.7-2.1). None of the patients had a need for dialysis. Median duration of hospital stay in CI-AKI patients was 15.0 days (2.5-97.5, percentile 1-92) after intra-arterial and 15.5 days (2.5-97.5, percentile 0-38) after intravenous contrast procedures. Renal function recovered after CI-AKI in 13/24 after intra-arterial and in 10/20 patients after intravenous contrast administration. Mortality risks in CI-AKI patients were slightly higher than in non-CI-AKI patients, hazard ratios 1.6 (95% CI 0.7-3.7) for intra-arterial and 1.7 (95% CI 0.7-4.4) for intravenous contrast administration, adjusted for confounders. Conclusion The risk of CI-AKI, and its clinical course was similar after intra-arterial and intravenous contrast media administration, after adjustment by design for patient-related risk factors.
Contrast-Induced Acute Kidney Injury: Short- and Long-Term Implications
Seminars in Nephrology, 2011
The intravascular administration of iodine-based contrast media remains a common cause of acute kidney injury and a leading cause of iatrogenic renal disease. Past research has elucidated the principal risk factors for contrast-induced acute kidney injury (CIAKI) and helped to establish the efficacy of various interventions for the prevention of this condition. The importance of preventing CIAKI has been underscored by a growing number of studies demonstrating strong associations of CIAKI with serious, adverse short and long-term outcomes. However, it remains unclear whether these associations are causal. This is important as considerable healthcare resources are used to prevent CIAKI. If CIAKI is a marker, but not a mediator, of serious, adverse downstream outcomes, more judicious and selective utilization of preventive care may be appropriate. Moreover, with an increasing number of studies reporting the under-utilization of coronary angiography in patients with acute coronary syndrome and underlying CKD, presumably due in part out of a fear of CIAKI, a clear understanding of whether this condition directly results in adverse downstream outcomes is essential. Careful inspection of past studies that investigated the association of CIAKI with adverse short and long-term events sheds light on their strengths and weaknesses and provides insight into how future research may be better able to characterize the short and long-term implications of this iatrogenic condition.
Italian Journal of Medicine, 2018
Contrast-induced acute kidney injury (CI-AKI) is defined as an acute kidney failure following iodine-based contrast medium administration determining relevant health and socio-sanitary implications. Knowledge of pathophysiology, early diagnosis, and prevention in patients at risk are critical points in CI-AKI management. Determination of risk and functional kidney evaluation must precede every iodine-based contrast medium (CM) administration in order to eventually introduce medical prophylaxis. Furthermore, early laboratoristic evaluation after iodine-based CM exposure should be performed for a prompt identification of acute kidney injury. Therefore, clinicians must know and strictly follow valid recommendations to minimize the development of complications.
Contrast-Induced Acute Kidney Injury
Journal of the American College of Cardiology, 2008
Cardiac angiography and coronary/vascular interventions depend on iodinated contrast media and consequently pose the risk of contrast-induced acute kidney injury (AKI). This is an important complication that accounts for a significant number of cases of hospital-acquired renal failure, with adverse effects on prognosis and health care costs. The epidemiology and pathogenesis of contrast-induced AKI, baseline renal function measurement, risk assessment, identification of high-risk patients, contrast medium use, and preventive strategies are discussed in this report. An advanced algorithm is suggested for the risk stratification and management of contrast-induced AKI as it relates to patients undergoing cardiovascular procedures. Contrast-induced AKI is likely to remain a significant challenge for cardiologists in the future because the patient population is aging and chronic kidney disease and diabetes are becoming more common.
Use of Intravenous Iodinated Contrast Media in Patients with Kidney Disease
Kidney Medicine
Intravenous iodinated contrast media are commonly used with CT to evaluate disease and to determine treatment response. The risk of acute kidney injury (AKI) developing in patients with reduced kidney function following exposure to intravenous iodinated contrast media has been overstated. This is due primarily to historic lack of control groups sufficient to separate contrast-induced AKI (CI-AKI; ie, AKI caused by contrast media administration) from contrast-associated AKI (CA-AKI; ie, AKI coincident to contrast media administration). Although the true risk of CI-AKI remains uncertain for patients with severe kidney disease, prophylaxis with intravenous normal saline is indicated for patients who have AKI or an estimated glomerular filtration rate less than 30 mL/min/1.73 m 2 who are not undergoing maintenance dialysis. In individual high-risk circumstances, prophylaxis may be considered in patients with an estimated glomerular filtration rate of 30-44 mL/min/1.73 m 2 at the discretion of the ordering clinician.
Preventing contrast medium-induced acute kidney injury
European Radiology, 2018
A side-by-side comparison of updated guidelines regarding contrast medium-induced acute kidney injury (CI-AKI) from the Swedish Society of Uroradiology (SSUR) and the European Society of Urogenital Radiology (ESUR) is presented. The major discrepancies include a higher glomerular filtration rate (GFR) threshold as a risk factor for CI-AKI and for discontinuation of metformin by SSUR, i.e., < 45 ml/min versus < 30 ml/min/1.73 m 2 by ESUR, when intravenous or intra-arterial contrast media (CM) with second-pass renal exposure is administered. SSUR also continues to recommend consideration of traditional non-renal risk factors such as diabetes and congestive heart failure, while ESUR considers these factors as non-specific for CI-AKI and does not recommend any consideration. Contrary to ESUR, SSUR also recommends discontinuation of NSAID and nephrotoxic medication if possible. Insufficient evidence at the present time motivates the more cautionary attitude taken by SSUR. Furthermore, SSUR expresses GFR thresholds in absolute values in ml/min as recommended by the National Kidney Foundation for drugs excreted by glomerular filtration, while ESUR uses the relative GFR normalised to body surface area in ml/min/1.73 m 2. CM dose/GFR ratio thresholds established for coronary angiography/interventions are also applied as recommendations for CM-enhanced CT by SSUR, since SSUR regards coronary procedures as a second-pass renal exposure of CM with no obvious difference in the incidence of AKI compared with IV CM administration. Finally, SSUR recommends reducing the gram-iodine dose/GFR ratio from < 1.0 in patients not at risk to < 0.5 in patients at risk of CI-AKI, while ESUR has no such recommendation. Key Points • The more cautionary attitude taken by SSUR compared with that of ESUR is motivated by insufficient evidence regarding risk for contrast medium-induced acute kidney injuries (CI-AKI). • SSUR recommends that absolute and not relative GFR should be used when dosing drugs eliminated by the kidneys such as contrast media. • According to SSUR the gram-iodine dose/GFR ratio should be < 0.5 in patients at risk of CI-AKI, while ESUR has no such recommendation.
Radiology Research and Practice, 2016
Background. Contrast induced nephropathy (CIN) is common cause of hospital acquired renal failure, defined as iatrogenic deterioration of renal function following intravascular contrast administration in the absence of another nephrotoxic event. Objectives. Objectives were to calculate incidence of CIN with routine IV contrast usage and to identify its risk factors. Materials and Methods. Study was conducted on 250 patients (having eGFR ≥ 45 mL/min/1.73 m 2) receiving intravenous contrast. Various clinical risk factors and details of contrast media were recorded. Patients showing 25% increase in postprocedural serum creatinine value or an absolute increase of 0.5 mg/dL (44.2 mmol/L) were diagnosed as having CIN. Results and Conclusions. Postprocedural serum creatinine showed significant increase from baseline levels. 25 patients (10%) developed CIN. CIN was transient in 21 (84%) patients developing CIN. One patient (4%) developed renal failure and another died due to unknown cause. Dehydration, preexisting renal disease, cardiac failure, previous contrast administration, and volume of contrast had significant correlation with development of CIN (< 0.05); whereas demographic variables, baseline serum creatinine/eGFR, previous renal surgery, diabetes mellitus, hypertension, nephrotoxic drug intake, abnormal routine hematology, and contrast characteristics had no correlation with CIN. CIN is a matter of concern even in routine imaging requiring intravenous contrast media, in our setup .
Prevention, Incidence, and Outcomes of Contrast-Induced Acute Kidney Injury
Archives of Internal Medicine, 2008
Background: Little is known about whether health care providers (physicians) implement preventive care for contrast-induced acute kidney injury (CIAKI). The objectives of our prospective cohort study were (1) to assess provider use of preventive strategies for CIAKI, (2) to determine the incidence of CIAKI, and (3) to examine the association of CIAKI with adverse outcomes at 30 days, including death, need for dialysis, and hospital admission. Methods: We prospectively identified patients with estimated glomerular filtration rates less than 60 mL/min/ 1.73 m 2 undergoing procedures with intravascular radiocontrast agents and recorded the use of intravenous fluids and N-acetylcysteine and the discontinuation of nonsteroidal anti-inflammatory medications. We measured postprocedure serum creatinine levels to quantify the incidence of CIAKI and tracked 30-day mortality and need for dialysis or hospitalization to evaluate the association of CIAKI with these outcomes. Results: Preprocedure and postprocedure intravenous fluids were administered to 264 of 660 study patients (40.0%), more commonly with coronary angiography than with computed tomography (91.2% vs 16.6%, PϽ.001). N-acetylcysteine was administered to 39.2% of patients, while only 6.8% of patients using nonsteroidal antiinflammatorydrugswereinstructedtodiscontinuethemedication. In a propensity analysis, the use of intravenous fluids was associated with a reduced rate of CIAKI. The incidence of CIAKI was lowest following computed tomography (range, 0.0%-10.9%) and was highest following noncoronary angiography (range, 1.9%-34.0%). Eleven patients (1.7%) died, 1 patient (0.2%) required dialysis, and 83 patients (12.6%) were hospitalized; however, CIAKI was not independently associated with hospital admission or death. Conclusions: Strategies to prevent CIAKI are implemented nonuniformly. Although biochemical evidence of CIAKI is relatively common, clinically significant CIAKI is rare. These findings should help health care providers focus the use of preventive care on the highest-risk patients and have important implications for future clinical trials.