Cellular pathophysiology of ischemic acute kidney injury
Joseph V. Bonventre, Li Yang
Joseph V. Bonventre, Li Yang
Published November 1, 2011
Citation Information: J Clin Invest. 2011;121(11):4210-4221. https://doi.org/10.1172/JCI45161.
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Category: Science in Medicine

Cellular pathophysiology of ischemic acute kidney injury

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

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Figure 5

Pathology after ischemia in humans.

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Pathology after ischemia in humans. (A) Outer medulla in human ischemic ...
(A) Outer medulla in human ischemic AKI. The proximal tubules (PT) lose brush border, and cells are released into the lumen (thin arrows). Inflammatory cells are seen in the interstitial compartment (thick arrow). Light microscopy: original magnification, ×400; scale bar: 50 μm. (B) Electron microscopy sections through normal human proximal tubules. (C–E) Human AKI. (C) In ischemic AKI, lymphocytes are seen infiltrating into the tubule wall (arrow). (D and E) Loss of brush border and contraction of the cell (arrow in D and dashed arrow in E) with necrosis (D and E) of proximal tubules are shown. Cellular debris is apparent in the lumen (solid arrows in E). Scale bars: 2 μm (B–E). TBM, tubular basement membrane.