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1 Division of Nephrology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA; Indiana Center for Biological Microscopy, Indiana University School of Medicine, Indianapolis, IN, USA
2 Division of Nephrology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA; Indiana Center for Biological Microscopy, Indiana University School of Medicine, Indianapolis, IN, USA; Roudebush VA Medical Center, Indianapolis, IN, USA
3 Division of Neonatology, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, USA
* To whom correspondence should be addressed. E-mail: tsutton2{at}iupui.edu.
The role of renal microvascular endothelial cell injury in the pathophysiology of ischemic acute renal failure (ARF) remains largely unknown. No consistent morphologic alterations have been ascribed to the endothelium of the renal microvasculature as a result of ischemia-reperfusion injury. Therefore, the purpose of this study was to examine biochemical markers of endothelial injury and morphologic changes of the renal microvascular endothelium in a rodent model of ischemic ARF. Circulating von Willebrand factor (vWF) was measured as a marker of endothelial injury. Twenty-four hours after ischemia, circulating vWF peaked at 124% over baseline values (p
0.001). The FVB-TIE2/GFP mouse was utilized to localize morphologic changes in the renal microvascular endothelium. Immediately following ischemia, there was a marked increase in F-actin aggregates in the basal and basolateral aspect of renal microvascular endothelial cells in the corticomedullary junction. Following 24 hours of reperfusion, the pattern of F-actin staining was more similar to that observed under physiologic conditions. In addition, alterations in the integrity of the adherens junctions of the renal microvasculature, as demonstrated by loss of localization in VE-cadherin immunostaining, were observed following 24 hours of reperfusion. This observation temporally correlated with the greatest extent of permeability defect in the renal microvasculature as identified using fluorescent dextrans and 2-photon intravital imaging. Taken together, these findings indicate that renal vascular endothelial injury occurs in ischemic ARF and may play an important role in the pathophysiology of ischemic ARF.
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