scholarly journals Radiology departmental policy compliance with Swedish guidelines regarding post-contrast acute kidney injury for examinations with iodinated contrast media

Radiography ◽  
2021 ◽  
Author(s):  
A. Bjällmark ◽  
M. Bazzi ◽  
M. Karlsson ◽  
E. Krakys ◽  
J. Kihlberg
Critical Care ◽  
2020 ◽  
Vol 24 (1) ◽  
Author(s):  
Karim Lakhal ◽  
Stephan Ehrmann ◽  
Vincent Robert-Edan

Abstract As we were taught, for decades, that iodinated contrast-induced acute kidney injury should be dreaded, considerable efforts were made to find out effective measures in mitigating the renal risk of iodinated contrast media. Imaging procedures were frequently either downgraded (unenhanced imaging) or deferred as clinicians felt that the renal risk pertaining to contrast administration outweighed the benefits of an enhanced imaging. However, could we have missed the point? Among the abundant literature about iodinated contrast-associated acute kidney injury, recent meaningful advances may help sort out facts from false beliefs. Hence, there is increasing evidence that the nephrotoxicity directly attributable to modern iodinated CM has been exaggerated. Failure to demonstrate a clear benefit from most of the tested prophylactic measures might be an indirect consequence. However, the toxic potential of iodinated contrast media is well established experimentally and should not be overlooked completely when making clinical decisions. We herein review these advances in disease and pathophysiologic understanding and the associated clinical crossroads through a typical case vignette in the critical care setting.


2020 ◽  
pp. 197140092097720
Author(s):  
Catarina Brito ◽  
Luís Falcão ◽  
Mário Raimundo ◽  
Sara Fernandes ◽  
Adriana Fernandes ◽  
...  

Purpose The potential nephrotoxicity of intravenous iodinated contrast media is a major concern for acute ischaemic stroke imaging evaluation. This study aimed to assess the incidence of acute kidney injury after intravenous iodinated contrast media exposure in acute ischaemic stroke patients. Methods We conducted a retrospective cohort analysis between January 2012 and July 2018 to select adult patients admitted to the emergency department with acute ischaemic stroke. The exposed patients received a uniform intravenous dose of low osmolar non-ionic iodinated contrast media, as part of the imaging protocol for acute ischaemic stroke. The unexposed patients underwent a non-enhanced cranial computed tomography scan. Acute kidney injury was defined according to the Kidney Disease Improving Global Outcomes criteria, limited to the first 72 hours. Results A total of 161 and 105 patients were included in the exposed and unexposed groups, respectively. The median age was 72.8 years (interquartile range 20), 53% were men and 97% were white. Demographic and baseline characteristics were similar between the groups. The incidence of acute kidney injury between exposed ( n = 10, 6.2%) and unexposed ( n = 1, 1%) groups ( P = 0.073) was similar and contrast exposure was not a significant predictor of acute kidney injury. Conclusion Intravenous iodinated contrast media exposure during acute ischaemic stroke imaging protocols is not an independent predictor of acute kidney injury in patients with normal or near-normal renal function. Studies with larger sample sizes would help to clarify if patients with both cardiovascular risk factors and impaired renal function could benefit from prophylactic measures.


2020 ◽  
Author(s):  
Hyewon Oh ◽  
Nieun Seo ◽  
Joon Seok Lim ◽  
Je Sung You ◽  
Yong Eun Chung

Abstract Post contrast-acute kidney injury (PC-AKI) is defined as the deterioration of renal function after administration of iodinated contrast media. The purpose of this study was to investigate the association between HMGB1 and PC-AKI and the protective effect of glycyrrhizin, a direct inhibitor of HMGB1, in rats. Rats were divided into three groups: control, PC-AKI and PC-AKI with glycyrrhizin. Oxidative stress, mRNA expressions of pro-inflammatory cytokines (IL-1α, IL-1β, IL-6 and TNF-α) and kidney injury markers (Kim-1, NGAL and IL-18) were assessed. In addition, the serum and intracellular protein levels of HMGB1 were analyzed. Moreover, serum creatinine (SCr), blood urea nitrogen (BUN) and lactate dehydrogenase (LDH) levels were assessed. Oxidative stress, pro-inflammatory cytokines, kidney injury markers and LDH were significantly higher in PC-AKI compared to the controls, but were lower in PC-AKI with glycyrrhizin. Intracellular and serum HMGB1 levels significantly increased after contrast media exposure, whereas they markedly decreased after glycyrrhizin pretreatment. SCr and BUN also decreased in PC-AKI with glycyrrhizin compared to PC-AKI. Our findings indicate that HMGB1 plays an important role in the development of PC-AKI and that glycyrrhizin has a protective effect against renal injury and dysfunction by inhibiting HMGB1 and reducing oxidative stress.


2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Tong-qiang Liu ◽  
Wei-li Luo ◽  
Xiao Tan ◽  
Yi Fang ◽  
Jing Chen ◽  
...  

Contrast-induced acute kidney injury (CI-AKI) is a serious complication in patients after administration of iodinated contrast media. Proper animal models of CI-AKI can help understand the mechanisms involved and prevent the disorder. We used the 5/6-nephrectomized (NE) rat to develop a CI-AKI model and to evaluate differences in the toxic effects on the kidney between iohexol and iodixanol. We found that six weeks after ablative surgery was the preferred time to induce CI-AKI. We compared multiple pretreatment plans and found that dehydration for 48 hours before iodixanol (320, 10 mL/kg) administration was optimal to induce CI-AKI in the 5/6 NE rats. Compared with iodixanol, iohexol induced a significantly greater reduction in renal function, severe renal tissue damage, intrarenal hypoxia, and apoptotic tubular cells. Iohexol and iodixanol resulted in similarly marked increases in levels of inflammation and oxidative stress. In summary, the 5/6 NE rat combined with dehydration for 48 hours is a useful pretreatment to establish a novel and reliable CI-AKI model. Iohexol induced more severe CI-AKI than iodixanol in this model.


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