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Abstract
Ischemic kidney injury often occurs in the context of multiple organ failure and sepsis. Here, we review the major components of this dynamic process, which involves hemodynamic alterations, inflammation, and endothelial and epithelial cell injury, followed by repair that can be adaptive and restore epithelial integrity or maladaptive, leading to chronic kidney disease. Better understanding of the cellular pathophysiological processes underlying kidney injury and repair will hopefully result in the design of more targeted therapies to prevent the injury, hasten repair, and minimize chronic progressive kidney disease.
Authors
Joseph V. Bonventre, Li Yang
Figure 2
Normal nephron, corticomedullary oxygen gradient, and outer medullary microvascular anatomy.
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(A ) Anatomy of nephron with regions identified. Outer medulla vasculature is shown with capillaries in red and venous system in blue. (B ) The vasa recta with countercurrent exchange of oxygen resulting in a gradient of decreasing oxygen tension.
Copyright © 2024 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)