• Childhood Kidney Diseases
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• v.19 no.2
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• pp.71-78
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• 2015

The incidence of acute kidney injury (AKI) in critically ill pediatric patients has been reported as increasing to 25 %, depending on population characteristics. The etiology of AKI has changed over the last 10-20 years from primary renal disease to the renal conditions associated with systemic illness. The AKI in pediatric population is associated with increased mortality and morbidity, and prevention is needed to reduce the consequence of AKI. It is known that the most important risk factors for AKI in critically ill pediatric patients are clinical conditions to be associated with decreased renal blood flow, direct renal injury, and illness severity. Renal hypoperfusion leads to neurohormonal activation including renin-angiotensin-aldosterone system, sympathetic nervous system, antidiuretic hormone, and prostaglandins. Prolonged renal hypoperfusion can result in acute tubular necrosis. The direct renal injury can be predisposed under the condition of renal hypoperfusion, and appropriate treatment of volume depletion is important to prevent AKI. The preventable causes of AKI include contrast-induced nephropathy, hemodynamic instability, inappropriate mediation use, and multiple nephrotoxic insults. Given the evidence of preventable factors for AKI, several actions such as the use of protocol for prevention of contrast-induced nephropathy, appropriate treatment of volume depletion, vigorous treatment of sepsis, avoidance of combinations of nephrotoxic medications, and monitoring of levels of drugs should be recommended.

• Childhood Kidney Diseases
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• v.23 no.2
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• pp.77-85
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• 2019

Contrast-associated acute kidney injury (CA-AKI) is a major concern when iodinated contrast material is administered, especially in patients at risk. Efforts have been undertaken to understand the detrimental effects of contrast media (CM). With the use of low-osmolar or iso-osmolar CM the incidence of CA-AKI has steadily decreased within the past decade; however, especially in the pediatric population information is scarce. Incidence rates have been reported to range between 0% to 18.75%, particularly depending on indication, selection of population (i.e. preexisting co-morbidities), and definition of AKI. Different biomarkers have been proposed, but confirmatory studies are either lacking or have contributed to their lack of diagnostic power. Proteomic approaches have been employed and may pave the way to such discovery. Prevention strategies have been tested and proposed, but the recently published AMACING and PRESERVE trials have shown that commonly used strategies (such as systematic hydration or administration of N-acetylcysteine) have no role in the prevention of CA-AKI. We propose that thoughtful assessment of one's fluid state is the most appropriate approach and depending on the hydration status diuretics or fluid administration should be provided to achieve an euvolemic state ahead of contrast exposure.

• Korean Circulation Journal
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• v.52 no.7
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• pp.485-495
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• 2022

Coronary artery disease is highly prevalent in chronic kidney disease (CKD) and is a risk factor for contrast-associated acute kidney injury (CA-AKI), a complication of cardiovascular procedures that require contrast administration (e.g., coronary angiography, percutaneous coronary intervention [PCI]). CA-AKI has a major impact on morbidity, mortality, and healthcare resource utilization. The incidence of CA-AKI is particularly high in patients with pre-existing CKD, advanced age and comorbidities that increase the likelihood of CKD. The focus of the present review is to provide a brief overview on the assessment of the risk for and prevention of CA-AKI in patients undergoing angiography and PCI, including recognition of the important patient- and procedure-related factors that may contribute to CA-AKI. Preventive and treatment strategies, the mainstay of which is volume repletion by normal saline, are briefly discussed. The main focus of the review is placed on technical details of contrast minimization techniques, including ultra-low contrast angiography and zerocontrast PCI. Operator competence in such techniques is important to ensure that procedural challenges in patients with CKD, like vessel calcification, multivessel disease and complex anatomical subsets, are effectively addressed by PCI while minimizing the risk of CA-AKI.

• Korean Journal of Radiology
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• v.25 no.3
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• pp.257-266
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• 2024

Objective: To investigate molecular and functional consequences of additional exposures to iodine- or gadolinium-based contrast agents within 24 hours from the initial intravenous administration of iodine-based contrast agents through an animal study. Materials and Methods: Fifty-six Sprague-Dawley male rats were equally divided into eight groups: negative control, positive control (PC) with single-dose administration of CT contrast agent, and additional administration of either CT or MR contrast agents 2, 4, or 24 hours from initial CT contrast agent injection. A 12 µL/g of iodinated contrast agent or a 0.47 µL/g of gadolinium-based contrast agent were injected into the tail vein. Serum levels of blood urea nitrogen, creatinine, cystatin C (Cys C), and malondialdehyde (MDA) were measured. mRNA and protein levels of kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) were evaluated. Results: Levels of serum creatinine (SCr) were significantly higher in repeated CT contrast agent injection groups than in PC (0.21 ± 0.02 mg/dL for PC; 0.40 ± 0.02, 0.34 ± 0.03, and 0.41 ± 0.10 mg/dL for 2-, 4-, and 24-hour interval groups, respectively; P < 0.001). There was no significant difference in the average Cys C and MDA levels between PC and repeated CT contrast agent injection groups (Cys C, P = 0.256-0.362; MDA, P > 0.99). Additional doses of MR contrast agent did not make significant changes compared to PC in SCr (P > 0.99), Cys C (P = 0.262), and MDA (P = 0.139-0.771) levels. mRNA and protein levels of KIM-1 and NGAL were not significantly different among additional CT or MR contrast agent groups (P > 0.05). Conclusion: A sufficient time interval, probably more than 24 hours, between repeated contrast-enhanced CT examinations may be necessary to avoid deterioration in renal function. However, conducting contrast-enhanced MRI on the same day as contrast-enhanced CT may not induce clinically significant kidney injury.

• Korean Journal of Radiology
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• v.22 no.9
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• pp.1547-1554
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• 2021

Objective: We aimed to investigate whether repeated intravascular administration of iodinated contrast media (ICM) or gadolinium-based contrast agents (GBCAs) within a short interval was associated with an increased risk of post-contrast acute kidney injury (PC-AKI). Materials and Methods: This retrospective study included 300 patients (mean age ± standard deviation, 68.5 ± 8.1 years; 131 male and 169 female) who had undergone at least one ICM-enhanced perfusion brain CT scan, had their baseline and follow-up serum creatinine levels available, and had not undergone additional contrast-enhanced examinations 72 hours before and after a time window of interest were included. The study population was divided into three groups: single-dose group and groups of patients who had received multiple contrast administrations in the time window of interest with the minimum contrast repeat interval either within 4 hours (0-4-hour group) or between 4 to 48 hours (4-48-hour group). Multivariable logistic regression analysis was conducted to evaluate the association between AKI and repeated ICM administrations. A similar supplementary analysis was performed including both ICM and GBCA. Results: When ICM was only considered ignoring GBCA, among 300 patients, 207 patients received a single dose of ICM, 58 had repeated doses within 4 hours (0-4-hour group), and 35 patients had repeated doses between 4 to 48 hours (4-48-hour group). Most patients (> 95%) had a baseline estimated glomerular filtration rate (eGFR) of ≥ 30 mL/min/1.73 m². AKI occurred in 7.2%, 13.8%, and 8.6% of patients in the single-dose, 0-4-hour, and 4-48-hour groups, respectively. In the 0-4-hour and 4-48-hour groups, additional exposure to ICM was not associated with AKI after adjusting for comorbidities and nephrotoxic drugs (all p values > 0.05). Conclusion: Repeated intravascular administrations of ICM within a short interval did not increase the risk of AKI in our study patients suspected of acute stroke with a baseline eGFR of ≥ 30 mL/min/1.73 m².

• Journal of The Korean Society of Clinical Toxicology
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• v.15 no.2
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• pp.122-130
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• 2017

Purpose: To evaluate the effects of low-dose intravenous N-acetylcysteine on the prevention of contrast-induced nephropathy (CIN) in patients undergoing computed tomography (CT). Methods: All patients presenting to our emergency department and undergoing CT with intravenous contrast media between August 2014 and April 2016 were retrospectively enrolled. We included hospitalized patients with renal dysfunction [estimated glomerular filtration rate (GFR) between 30 and $89mL/min/1.73m^2$]. A 600-mg injection of N-acetylcysteine was given to patients once before and once immediately after CT, depending on the preference of physician. The primary outcome was CIN defined as an increase in creatinine level of ${\geq}25%$ or ${\geq}0.5mg/dL$ from the baseline within 48 to 72 hours after CT. A trained person blindly reviewed all medical records. Results: Of the 1903 admitted patients, CIN occurred in 9.8% of patients who received 1200 mg intravenous N-acetylcysteine (24/244) and 6.8% of patients who did not (113/1659, p=0.090). In a multivariable regression analysis, N-acetylcystine was not relevant to the prevention of CIN (odds ratio=1.42 [95% CI, 0.90-2.26]). Even in the stratified analysis using the propensity score matching, N-acetylcysteine was irrelevant (GFR 30-59: odds ratio=1.06 [95% CI, 0.43-2.60]; GFR 60-89: odds ratio=1.76 [95% CI, 0.75-4.14]). After adjustment, crystalloids were significantly associated with the reduction in CIN compared with dextrose water (odds ratio=0.60 [95% CI, 0.37-0.97]). Conclusion: No effect was found when low-dose intravenous N-acetylcysteine was used to prevent CIN. However, there seems to be an association between crystalloids and reduction in CIN.

• Tuberculosis and Respiratory Diseases
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• v.74 no.4
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• pp.163-168
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• 2013

Background: In uncontrolled hemoptysis patient, bronchial arteriography and bronchial artery embolization (BAE) is a important procedure in diagnosis and treatment. The aim of this study is to assess the incidence of contrast-induced nephropathy and the risk factors of contrast-induced nephropathy (CIN) after bronchial arteriography and BAE. Methods: We retrospectively reviewed the medical records of the patients who underwent bronchial arteriography and BAE in two university hospitals from January 2003 to December 2011. CIN was defined as rise of serum creatinine more than 25% of baseline value or 0.5 mg/dL at between 48 hours and 96 hours after bronchial arteriography and BAE. We excluded patients who already had severe renal insufficiency (serum creatinine${\geq}4.0$) or had been receiving dialysis. Results: Of the total 100 screened patients, 88 patients met the enrollment criteria. CIN developed in 7 patients (8.0%). The mean duration between the exposure and development of CIN was $2.35{\pm}0.81$ days. By using multivariate analysis, serum albumin level was found to be significantly associated with the development of CIN (p=0.0219). Conclusion: These findings suggest that the incidence of CIN was higher than expected and patients with hypoalbuminemia should be monitored more carefully to prevent the development of CIN after bronchial arteriography and BAE.