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. 2023 Jul 3;39(2):383–395. doi: 10.1007/s00467-023-06039-0

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Kidney development, repair, and regeneration. Development: In kidney development, growth and branching of ureteric bud (UB) is influenced by the kidney stem/progenitor cell population localized at the cap mesenchyme (CM). With branching of UB, renal vesicles (RV) emerge by pre-tubular aggregates. Specific genes are upregulated only during nephrogenesis including SIX1, SIX2, CITED1, OSR1, LGR5, GDNF, and RET. Repair: After AKI, epithelial cells will dedifferentiate, proliferate, and redifferentiate to form new tubular cells. If the epithelial cells fail to fully re-differentiate, maladaptive repair will occur. Maladaptive repair will cause fibrosis, inflammation, and senescence which will eventually lead to CKD. Regeneration: Genes related to human development including PAX2, LHX1, and SOX9 are re-expressed in injured tubular cells during regeneration. However, specific nephrogenesis genes are not upregulated in regeneration, and therefore, complementary therapy is required