Summary: 

AKI is a common complication in hospitalized patients, and studies have shown that T cells are frequently responsible for the pathogenic processes underlying AKI.  However, the exact mechanisms and micro environments that promote AKI is not well understood. The goal of this article review was to further evaluate the underlying pathogenesis of AKI and identify the underlying molecular process that promote AKI, as better understanding of the underlying molecular process may offer potential targets for future therapies. This article specifically identified TIGIT, a transmembrane glycoprotein in memory and activated T cells and NK cells, as a protein that is upregulated in kidney T cells in the setting of both murine and human AKI. The article suggests that increased TIGIT expression promotes the release of inflammatory cytokines Further evaluation showed TIGIT expression to promote a proinflammatory state that mediates ischemic any nephrotoxic AKI in the experimental sudden. TIGIT may be a possible future target for AKI therapies. 

Objectives:

At the conclusion of this activity, the learner should be able to:

• Demonstrate a potential mechanism by which T cells mediate AKI
• Recognize the role of TIGIT expression in promoting inflammation and contributing to AKI
• Illustrate different pathophysiologic processes that contribute to AKI
• Identify potential future targets for novel AKI therapies

Bio:

Haley Meyer, M.D.

Originally from St. Louis, MO. Completed undergraduate education and medical school in Chicago before coming to Mayo for Internal Medicine Residency. Plan to pursue heme-onc fellowship.

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TRANSCRIPT
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