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Translational Nephrology: Taking Aim at Tubular Debris

Acute kidney injury is characterized by a rapid decline in renal function, which results in the accumulation of metabolic waste and toxins. Changes that result in decreased renal blood flow or the presence of toxic chemicals (e.g. metabolic by-products from medications) within the blood can cause stress to the tubular cells within the kidney, whose task is to reabsorb metabolites before they are excreted in the urine. If the stress persists, tubular cells will die. The loss of cells within the tubules decreases the kidneys capacity for reabsorption, and the debris produced by dying cells can result in blockage of the tubules, resulting in decreased flow. The combination of these factors within the nephrons, decreased flow, increased renal protein, high salt, and low pH create ideal conditions for cast formation, which can further complicate matters. Therefore, mechanisms are needed to ensure efficient clearance of debris in order to initiate repair and restore kidney function. In their recent paper, Arai et al. (Nat. Med. 2016; 22: 183-193), have identify one such mechanism involving the Apoptosis Inhibitor of Macrophages protein (AIM). In the blood of healthy individuals, AIM can be found in complexes with IgM. The presence of inflammation induces the release of AIM, which then enters into the tubules within the kidney to mark debris for disposal by phagocytes. Activated tubular cells, which are undergoing proliferation in order to replace lost cells, upregulate a receptor that binds AIMtagged debris. The receptor is called Kidney Injury Molecule 1 (KIM-1) and bestows upon the surviving tubular cells the ability to repair tubular function much like a do-it-yourself (DIY) kit. Best of all, it appears that the application of recombinant AIM during AKI may be of therapeutic benefit for improving kidney function.


Jonathan A. Lindquist and Peter R. Mertens

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