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Kidney surveillance in the spotlight: contrast-induced acute kidney injury illuminated
Simon J. Atkinson
Simon J. Atkinson
Published June 4, 2018
Citation Information: J Clin Invest. 2018;128(7):2754-2756. https://doi.org/10.1172/JCI121741.
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Commentary

Kidney surveillance in the spotlight: contrast-induced acute kidney injury illuminated

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Abstract

Acute kidney injury comprises a heterogeneous group of conditions characterized by a sudden decrease in renal function over hours to days. Contrast-induced acute kidney injury (CI-AKI) is caused by radiographic contrast agents used in diagnostic imaging. In the current issue of the JCI, Lau et al. use a mouse model of CI-AKI to study the role of resident and infiltrating phagocytes, recruited leukocytes, and tubular cells in the immune surveillance response to contrast agents. This study has the potential to provide innovative therapies for human CI-AKI.

Authors

Simon J. Atkinson

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Figure 1

Dependence of contrast distribution and immune activation on volume status.

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Dependence of contrast distribution and immune activation on volume stat...
In the hydrated state (A), contrast is filtered and passes into the tubule lumen but does not accumulate and is not reabsorbed. Consequently, the inflammasome in infiltrating leukocytes is not stimulated, and there is insufficient immune activation to induce a prolific leukocyte infiltration and strong inflammatory response. In contrast (B), in the volume-depleted state, filtered contrast accumulates in the tubule lumen and is reabsorbed, resulting in stimulation of infiltrating leukocytes in addition to resident macrophages, leading to a massive influx of leukocytes and an excessive inflammatory response that ultimately precipitates AKI. DPEP-1, dipeptidase-1.
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