Gadolinium-based contrast media exposure and the possible risk of subclinical kidney damage: a pilot study

Martino, Francesca; Amici, Gianpaolo; Godi, Ilaria; Baretta, Michele; Biasi, Caterina; Carta, M.; Corradi, Valentina; Cal, Massimo de; Knust, Maira; Tamayod, Claudia; Varotto, Alessia; Iannucci, Giuseppe; Giavarina, Davide; Savastano, Sergio; Ronco, Claudio

doi:10.1007/s11255-020-02779-2

Cited by 3 publications

(3 citation statements)

References 20 publications

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“…Most researchers agree that the contrast agents used for CT and MRI have different risk profiles for kidney injury. Therefore, the subgroup analysis by the type of imaging examinations (CT/MRI) was performed and the results clarified that the increased risk attributed to exposure iodine-based contrast medium in CT instead of gadolinium-based contrast media, which was consistent with previous findings that gadolinium-based contrast media generally leads to subclinical kidney damage without any significant modification of SCr [6,7]. The aRR for the risk of AKI after exposure to gadolinium-based contrast media was more than 1, although 95% CI included 1, which remand us the potential kidney injury of gadolinium-based contrast did not be ignored.…”

Section: Discussionsupporting

confidence: 84%

“…However, the impacts of intravenous iodinebased contrast on renal function, including renal tubular epithelial cells damage and hemodynamic perturbations induced by contrast media, are still a research hotspot [2][3][4]. Although initially believed to be without major adverse effects, gadolinium-based contrast agents was demonstrated to cause nephrogenic systemic fibrosis in patients with abnormal renal function [5]; moreover, a recent study indicated that exposure to Gadolinium was related to both necrosis and apoptosis of proximal tubular epithelium which led to kidney injury after Gadolinium exposure [6,7]. A retrospective study found that sequential exposure to iodine-and gadolinium-based contrast media on the same admission was a risk factors for post-contrast acute kidney injury (AKI) [1].…”

Section: Introductionmentioning

confidence: 99%

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Risk of acute kidney injury following contrast-enhanced CT or MRI in a cohort of 3061 hospitalized children in China

Wang,

Zhang,

Sun

et al. 2024

BMC Pediatr

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Objectives To compare the risk of acute kidney injury (AKI) between hospitalized children who received intravenous contrast media for imaging examinations and those who did not. Methods This retrospective cohort study enrolled patients aged 0–18 years with serum creatinine levels before and after imaging examinations from 2015 to 2020 at Beijing Children’s Hospital. Participants were classified into an exposure group or a control group. Log-binomial regression analysis was used to estimate the adjusted risk ratio (aRR) value for the association between exposure to contrast media and consequential AKI. After which, inverse probability treatment weighting was used to reduce systematic differences in baseline characteristics among the groups. Moreover, subgroup and sensitivity analyses were performed. Finally, multivariate logistic regression analysis was performed to identify risk factors for pediatric AKI. Results In total, 3061 pediatric patients were included in the analyses (median age, 4.5 [IQR, 1.3–8.9] years, 1760 males). According the KDIGO definition of AKI, the incidence of AKI in the exposure group, and the control group were 7.4% and 6.5%, respectively; furthermore, the aRR was 1.35 (95% CI: 1.31–1.39). In patients underwent CT, the risk of AKI in the exposure group of contrast media increased compared with the control group and the aRR was 1.39 (95% CI: 1.09–1.78). However, it is not observed in patients underwent MRI (aRR: 1.36; 95% CI: 0.96–1.95). According to our subgroup analysis of pediatric patients aged ≥ 2 years (aRR: 1.38; 95% CI: 1.05–1.82) and sensitivity analysis (aRR: 1.32, 95% CI: 1.08–1.61), the risk of AKI in the exposure group was greater than that in the control group. An increased risk to exposure to contrast media was seen in females (aRR: 1.41, 95% CI: 1.05–1.89) rather than males (aRR: 1.30, 95% CI: 0.99–1.70). According to the multivariate logistic regression analyses, the baseline eGFR (OR: 1.02; 95% CI: 1.01–1.03) and comorbidities (OR: 2.97; 95% CI: 1.89–4.65) were risk factors, while age (OR: 0.87; 95% CI: 0.84–0.91) was a protective factor against AKI. Conclusion The evidence from the present study suggested that the increased risk of AKI in hospitalized children induced by intravascular contrast should not be ignored.

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Section: Discussionsupporting

confidence: 84%

Section: Introductionmentioning

confidence: 99%

Risk of acute kidney injury following contrast-enhanced CT or MRI in a cohort of 3061 hospitalized children in China

Wang,

Zhang,

Sun

et al. 2024

BMC Pediatr

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“…Until the mid-2000s, gadolinium-enhanced magnetic resonance imaging (MRI) was a preferred imaging modality in patients with advanced kidney disease. Although there is some evidence for direct gadolinium nephrotoxicity, current evidence suggests that gadolinium, when used at typical clinical doses, imparts minimal risk for significant AKI (83). However, studies have linked gadolinium-based contrast agents (GBCAs) with the development of nephrogenic systemic fibrosis (NSF), an often debilitating fibrosing disorder of skin, connective tissue, and, in certain cases, internal organs in patients with significantly impaired kidney function (84)(85)(86).…”

Section: Gadolinium-based Contrast and Nephrogenic Systemic Fibrosismentioning

confidence: 99%

Radiographic Contrast Media and the Kidney

Cashion

Weisbord

2022

CJASN

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AKI is a potential complication of intravascular iodinated contrast exposure. Contrast-associated AKI, which typically manifests as small and transient decrements in kidney function that develop within several days of contrast administration, is associated with serious adverse outcomes, including progressive kidney dysfunction and death. However, a causal link between the small increases in serum creatinine that characteristically occur with contrast-associated AKI and serious adverse outcomes remains unproven. This is important given mounting evidence that clinically indicated, potentially lifesaving radiographic procedures are underutilized in patients with CKD. This has been hypothesized to be related to provider concern about precipitating contrast-associated AKI. Intravascular gadolinium-based contrast, an alternative to iodinated contrast that is administered with magnetic resonance imaging, has also been linked with potential serious adverse events, notably the development of nephrogenic systemic fibrosis in patients with severe impairment in kidney function. Patients hospitalized in the intensive care unit frequently have clinical indications for diagnostic and therapeutic procedures that involve the intravascular administration of contrast media. Accordingly, critical care providers and others treating critically ill patients should possess a sound understanding of the risk factors for and incidence of such outcomes, the ability to perform evidence-based risk-benefit assessments regarding intravascular contrast administration, and knowledge of empirical data on the prevention of these iatrogenic complications.

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Role of uranium toxicity and uranium-induced oxidative stress in advancing kidney injury and endothelial inflammation in rats

Yang,

Dai,

Chen

et al. 2024

BMC Pharmacol Toxicol

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Objective Uranium exposure may cause serious pathological injury to the body, which is attributed to oxidative stress and inflammation. However, the pathogenesis of uranium toxicity has not been clarified. Here, we evaluated the level of oxidative stress to determine the relationship between uranium exposure, nephrotoxic oxidative stress, and endothelial inflammation. Methods Forty male Sprague–Dawley rats were divided into three experimental groups (U-24h, U-48h, and U-72h) and one control group. The three experimental groups were intraperitoneally injected with 2.0 mg/kg uranyl acetate, and tissue and serum samples were collected after 24, 48, and 72 h, respectively, whereas the control group was intraperitoneally injected with 1.0 ml/kg normal saline and samples were collected after 24 h. Then, we observed changes in the uranium levels and oxidative stress parameters, including the total oxidative state (TOS), total antioxidant state (TAS), and oxidative stress index (OSI) in kidney tissue and serum. We also detected the markers of kidney injury, namely urea (Ure), creatine (Cre), cystatin C (CysC), and neutrophil gelatinase-associated lipocalin (NGAL). The endothelial inflammatory markers, namely C-reactive protein (CRP), lipoprotein phospholipase A2 (Lp-PLA2), and homocysteine (Hcy), were also quantified. Finally, we analyzed the relationship among these parameters. Results TOS (z = 3.949; P < 0.001), OSI (z = 5.576; P < 0.001), Ure (z = 3.559; P < 0.001), Cre (z = 3.476; P < 0.001), CysC (z = 4.052; P < 0.001), NGAL (z = 3.661; P < 0.001), and CRP (z = 5.286; P < 0.001) gradually increased after uranium exposure, whereas TAS (z = −3.823; P < 0.001), tissue U (z = −2.736; P = 0.001), Hcy (z = −2.794; P = 0.005), and Lp-PLA2 (z = −4.515; P < 0.001) gradually decreased. The serum U level showed a V-shape change (z = −1.655; P = 0.094). The uranium levels in the kidney tissue and serum were positively correlated with TOS (r = 0.440 and 0.424; P = 0.005 and 0.007) and OSI (r = 0.389 and 0.449; P = 0.013 and 0.004); however, serum U levels were negatively correlated with TAS (r = −0.349; P = 0.027). Partial correlation analysis revealed that NGAL was closely correlated to tissue U (rpartial = 0.455; P = 0.003), CysC was closely correlated to serum U (rpartial = 0.501; P = 0.001), and Lp-PLA2 was closely correlated to TOS (rpartial = 0.391; P = 0.014), TAS (rpartial = 0.569; P < 0.001), and OSI (rpartial = −0.494; P = 0.001). Pearson correlation analysis indicated that the Hcy levels were negatively correlated with tissue U (r = −0.344; P = 0.030) and positively correlated with TAS (r = 0.396; P = 0.011). Conclusion The uranium-induced oxidative injury may be mainly reflected in enhanced endothelial inflammation, and the direct chemical toxicity of uranium plays an important role in the process of kidney injury, especially in renal tubular injury. In addition, CysC may be a sensitive marker reflecting the nephrotoxicity of uranium; however, Hcy is not suitable for evaluating short-term endothelial inflammation involving oxidative stress.

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Gadolinium-based contrast media exposure and the possible risk of subclinical kidney damage: a pilot study

Cited by 3 publications

References 20 publications

Risk of acute kidney injury following contrast-enhanced CT or MRI in a cohort of 3061 hospitalized children in China

Risk of acute kidney injury following contrast-enhanced CT or MRI in a cohort of 3061 hospitalized children in China

Radiographic Contrast Media and the Kidney

Role of uranium toxicity and uranium-induced oxidative stress in advancing kidney injury and endothelial inflammation in rats

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