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Multiparametric MRI assessment of renal structure and function in acute kidney injury and renal recovery

BACKGROUND: Acute kidney injury (AKI) is associated with a marked increase in mortality as well as subsequent chronic kidney disease (CKD) and end-stage kidney disease. We performed multiparametric magnetic resonance imaging (MRI) with the aim of identifying potential non-invasive MRI markers of ren...

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Detalles Bibliográficos
Autores principales: Buchanan, Charlotte, Mahmoud, Huda, Cox, Eleanor, Noble, Rebecca, Prestwich, Benjamin, Kasmi, Isma, Taal, Maarten W, Francis, Susan, Selby, Nicholas M
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8323137/
https://www.ncbi.nlm.nih.gov/pubmed/34345421
http://dx.doi.org/10.1093/ckj/sfaa221
Descripción
Sumario:BACKGROUND: Acute kidney injury (AKI) is associated with a marked increase in mortality as well as subsequent chronic kidney disease (CKD) and end-stage kidney disease. We performed multiparametric magnetic resonance imaging (MRI) with the aim of identifying potential non-invasive MRI markers of renal pathophysiology in AKI and during recovery. METHODS: Nine participants underwent inpatient MRI scans at time of AKI; seven had follow-up scans at 3 months and 1 year following AKI. Multiparametric renal MRI assessed total kidney volume (TKV), renal perfusion using arterial spin labelling, T(1) mapping and blood oxygen level-dependent (BOLD) R(2)* mapping. RESULTS: Serum creatinine concentration had recovered to baseline levels at 1-year post-AKI in all participants. At the time of AKI, participants had increased TKV, increased cortex/medulla T(1) and reduced cortical perfusion compared with the expected ranges in healthy volunteers and people with CKD. TKV and T(1) values decreased over time after AKI and returned to expected values in most but not all patients by 1 year. Cortical perfusion improved to a lesser extent and remained below the expected range in the majority of patients by 1-year post-AKI. BOLD R(2)* data showed a non-significant trend to increase over time post-AKI. CONCLUSIONS: We observed a substantial increase in TKV and T(1) during AKI and a marked decrease in cortical perfusion. Despite biochemical recovery at 1-year post-AKI, MRI measures indicated persisting abnormalities in some patients. We propose that such patients may be more likely to have further AKI episodes or progress to CKD and further longitudinal studies are required to investigate this.