ArticleBMC nephrology2025
Diffusion kurtosis imaging and arterial spin labeling MRI for assessment of post-contrast acute kidney injury risk in rats with subclinical kidney injury.
Article in BMC nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundThe risk of post-contrast acute kidney injury (PC-AKI) following subclinical acute kidney injury (sAKI) remains unclear. This study was performed to determine whether sAKI increases the risk of PC-AKI and to assess the utility of multiparametric MRI, including diffusion kurtosis imaging (DKI) and arterial spin labeling (ASL), for detecting pathological changes with high sensitivity.
methodsA rat model of subclinical kidney injury was established through subcutaneous injection of carbon tetrachloride for 6 weeks. Subclinical kidney injury and control groups (n = 30 each) received intravascular iopamidol (4 g iodine/kg). Kidney MRI, including DKI and ASL, was conducted at 24 h before and at 1, 24, 48, and 72 h after iopamidol administration (n = 6 per time point). Key parameters measured included renal mean kurtosis (MK), mean diffusion (MD), renal blood flow (RBF), blood urea nitrogen (BUN), serum creatinine (SCr), histopathological changes assessed by hematoxylin-eosin (HE) score, hypoxia-inducible factor-1α (HIF-1α) expression, and renal tissue neutrophil gelatinase-associated lipocalin (NGAL) expression.
resultsAt baseline, the subclinical kidney injury group showed higher mRNA expression of renal NGAL, increased HE scores, and a greater HIF-1α-positive area in all renal compartments compared with controls. Additionally, MD in the outer stripe of the outer medulla (OSOM) and RBF were lower in the subclinical kidney injury group than in the control group. At 1 h after iopamidol injection, HE scores, NGAL expression, and HIF-1α expression further increased, whereas MD and RBF further decreased in both groups compared with their respective baselines. At 24 h in the control group, all indicators returned to baseline levels, but changes in the subclinical kidney injury group persisted. By 48 and 72 h, all indicators in both groups had returned to baseline levels. SCr and BUN levels remained unchanged in the control group at all time points but increased at 1 and 24 h in the subclinical kidney injury group. MRI parameters showed strong correlations with histopathological findings and NGAL expression.
conclusionsRats with subclinical kidney injury exhibited more severe PC-AKI and slower resolution of microstructural and oxygenation changes compared with controls.
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