Abstract
Background/Objectives: Gadolinium-based contrast agents (GBCA) are widely used in magnetic resonance imaging and are generally considered to have a lower potential for nephrotoxicity compared to iodinated contrast agents. However, the actual prevalence of acute kidney injury (AKI) following the use of GBCA and the risk factors contributing to it remain a subject of debate today. The aim of this study is to determine the incidence of acute kidney injury following gadolinium administration (AKI-FGA) in patients undergoing contrast-enhanced magnetic resonance imaging (MRI) and to evaluate the independent risk factors contributing to it. Methods: The medical records of all patients who underwent contrast-enhanced MRI at our hospital between January 2021 and December 2022 were retrospectively reviewed. The patients’ demographic characteristics and serum creatinine levels before and after the contrast-enhanced MRI examination were evaluated. Contrast-induced acute kidney injury (AKI) was defined according to the Kidney Disease: Improving Global Outcomes (KDIGO) criteria as an increase in serum creatinine of ≥0.3 mg/dL within 48 hours following contrast agent administration or a rise to ≥1.5 times the baseline value within 7 days. Patients who met the KDIGO criteria were included in the AKI-FGA group. Results: A total of 503 patients who met the inclusion criteria were enrolled in the study. The mean age of the patients was 60.88 ± 16.83 years, and 60.4% of the patients (n=304) were male. Following GBCA administration, a statistically significant increase in serum urea and creatinine levels and a significant decrease in eGFR were observed (p=0.001). AKI-FGA was detected in 16.5% of the patients (n=83). In the AKI-FGA group, the number of patients with a history of coronary artery disease (CAD), diabetes mellitus (DM), hypertension (HT), and congestive heart failure (CHF) was statistically significantly higher than in the group without AKI-FGA (p<0.05). In the multivariate analysis, each 1-year increase in age increased the risk of AKI-FGA by a factor of 1.03, each 0.1 mg/dL increase in baseline serum creatinine increased it by a factor of approximately 4.96, and the presence of DM and CHF increased it by factors of 2.16 and 2.92, respectively. In contrast, no statistically significant association was found between the development of AKI-FGA and HT or CAD. Conclusions: Our findings demonstrate that acute kidney injury can develop following contrast-enhanced MRI even in patients without a history of kidney disease. In particular, for patients who are elderly or have DM, CHF, or elevated baseline serum creatinine levels, it is clinically important to perform an individualized risk assessment prior to contrast-enhanced MRI and to closely monitor kidney function following the procedure.