Abstract
To characterize ischemia reperfusion injury (IRI)-induced acute kidney injury (AKI) in C57BL/6 (B6) and CD1-mice by longitudinal functional MRI-measurement of edema formation (T2-mapping) and inflammation (diffusion weighted imaging (DWI)). IRI was induced with unilateral right renal pedicle clamping for 35min. 7T-MRI was performed 1 and 14 days after surgery. DWI (7 b-values) and multiecho TSE sequences (7 TE) were acquired. Parameters were quantified in relation to the contralateral kidney on day 1 (d1). Renal MCP-1 and IL-6-levels were measured by qPCR and serum-CXCL13 by ELISA. Immunohistochemistry for fibronectin and collagen-4 was performed. T2-increase on d1 was higher in the renal cortex (127 ± 5% vs. 94 ± 6%, p < 0.01) and the outer stripe of the outer medulla (141 ± 9% vs. 111 ± 9%, p < 0.05) in CD1, indicating tissue edema. Medullary diffusivity was more restricted in CD1 than B6 (d1: 73 ± 3% vs. 90 ± 2%, p < 0.01 and d14: 77 ± 5% vs. 98 ± 3%, p < 0.01). Renal MCP-1 and IL-6-expression as well as systemic CXCL13-release were pronounced in CD1 on d1 after IRI. Renal fibrosis was detected in CD1 on d14. T2-increase and ADC-reduction on d1 correlated with kidney volume loss on d14 (r = 0.7, p < 0.05; r = 0.6, p < 0.05) and could serve as predictive markers. T2-mapping and DWI evidenced higher susceptibility to ischemic AKI in CD1 compared to B6.
Highlights
Relative ADC values decreased on d1 after acute kidney injury (AKI) in both mouse strains and remained at reduced levels two weeks after ischemia reperfusion injury (IRI) (Figure 1)
We could show that Diffusion weighted imaging (DWI) and T2 mapping allow for the monitoring of pathophysiological changes after renal IRI
Tissue water content and infiltration of inflammatory cells are hallmarks of IRI and can be quantified by functional magnetic resonance imaging (MRI). It has been demonstrated in a previous study that CD1 mice have an increased susceptibility to renal IRI compared to B6 mice [9]
Summary
Acute kidney injury (AKI) due to ischemia reperfusion injury (IRI) is common in many clinical situations including cardiac surgery and hemodynamic instability [1]. AKI is associated with an increased risk for progression to chronic kidney disease (CKD) and poor patient outcome [2,3]. Several other risk factors for the development and aggravation of AKI have been identified such as hypertension, diabetes or drug related side-effects [4,5]. C57BL/6 (B6) mice are a commonly used mouse strain for IRI-induced AKI studies and background for many genetic knockout models in renal IRI [6,7]. A recent study used functional MRI in CD1 mice and found that they exhibit pronounced renal
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