Skip to main content
. Author manuscript; available in PMC: 2019 Feb 1.
Published in final edited form as: Acta Physiol (Oxf). 2017 Jul 25;222(2):10.1111/apha.12914. doi: 10.1111/apha.12914

Figure 1.

Figure 1

Alterations in endothelial function contribute to the extension phase of acute kidney injury. On the left, a peritubular capillary is shown in close apposition to tubular epithelium in a normal kidney. B) In response to injury, endothelial swelling narrows capillary space. Increased adhesion molecule expression facilitates leukocyte attachment, contributing to erythrocyte rouleaux formation and disrupting normal blood flow. Reduction in flow contributes to reduced shear stress and inhibition of NO formation, a potential trigger for endothelial mesenchymal transition (EndoMT). Addition potential contributors toward EndoMT include a reduction in trophic support from damaged tubules or injury activated perictyes. Disruption of blood flow exacerbates tissue hypoxia and further compromises epithelial injury and a reduction in renal