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AKI-to-CKD Transition

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Acute Kidney Injury and Regenerative Medicine

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Abstract

Previously conceived to be a benign syndrome, AKI has now proven to be one important cause of CKD. So far, eight kinds of rodent models have been introduced to the basic research model for the AKI-to-CKD transition. Among these, the unilateral ischemia-reperfusion injury (uIRI) and repeated low-dose cisplatin (RLDC) models were proposed as consistent rodent models for the AKI-to-CKD transition. However, these two rodent models demonstrate divergent data on kidney injury, and an easy and accurate way of monitoring renal function will be needed. In the proposed mechanism, renal hypoxia plays a pivotal role in the AKI-to-CKD transition with capillary rarefaction, abnormally differentiated tubular cells, epigenetic changes in fibroblasts, and persisting inflammation.

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Authors and Affiliations

  1. Department of Nephrology, Osaka University Graduate School of Medicine, Osaka, Japan

    Jun-Ya Kaimori

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  1. Jun-Ya Kaimori
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Correspondence to Jun-Ya Kaimori .

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  1. Department of Endocrinology, Metabolism, and Nephrology, Kochi Medical School, Kochi University, Nankoku, Kochi, Japan

    Yoshio Terada

  2. Department of Nephrology and Laboratory Medicine, Kanazawa University, Kanazawa, Ishikawa, Japan

    Takashi Wada

  3. Department of Acute Medicine, The University of Tokyo, Tokyo, Japan

    Kent Doi

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Kaimori, JY. (2020). AKI-to-CKD Transition. In: Terada, Y., Wada, T., Doi, K. (eds) Acute Kidney Injury and Regenerative Medicine . Springer, Singapore. https://doi.org/10.1007/978-981-15-1108-0_20

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