AKI affects approximately 13.3 million people around the world each year, causing CKD and/or mortality. The mammalian kidney cannot generate new nephrons after postnatal renal damage and regenerative therapies for AKI are not available. Human kidney tissue culture systems can complement animal models of AKI and/or address some of their limitations. Donor-derived somatic cells, such as renal tubule epithelial cells or cell lines (RPTEC/hTERT, ciPTEC, HK-2, Nki-2, and CIHP-1), have been used for decades to permit drug toxicity screening and studies into potential AKI mechanisms. However, tubule cell lines do not fully recapitulate tubular epithelial cell properties in situ when grown under classic tissue culture conditions. Improving tissue culture models of AKI would increase our understanding of the mechanisms, leading to new therapeutics. Human pluripotent stem cells (hPSCs) can be differentiated into kidney organoids and various renal cell types. Injury to human kidney organoids results in renal cell-type crosstalk and upregulation of kidney injury biomarkers that are difficult to induce in primary tubule cell cultures. However, current protocols produce kidney organoids that are not mature and contain off-target cell types. Promising bioengineering techniques, such as bioprinting and "kidney-on-a-chip" methods, as applied to kidney nephrotoxicity modeling advantages and limitations are discussed. This review explores the mechanisms and detection of AKI in tissue culture, with an emphasis on bioengineered approaches such as human kidney organoid models.

AKI 每年影响全球约 1330 万人，导致 CKD 和/或死亡。哺乳动物肾脏在产后肾损伤后不能产生新的肾单位，并且 AKI 的再生疗法不可用。人类肾脏组织培养系统可以补充 AKI 动物模型和/或解决它们的一些局限性。几十年来，供体来源的体细胞，如肾小管上皮细胞或细胞系（RPTEC/hTERT、ciPTEC、HK-2、Nki-2 和 CIHP-1）已被用于药物毒性筛选和潜在研究AKI 机制。然而，肾小管细胞系并不能完全再现肾小管上皮细胞的原位特性当在经典组织培养条件下生长时。改进 AKI 的组织培养模型将增加我们对机制的理解，从而产生新的治疗方法。人多能干细胞 (hPSC) 可以分化为肾类器官和各种肾细胞类型。人肾类器官的损伤导致肾细胞类型串扰和肾损伤生物标志物的上调，这在原代肾小管细胞培养物中难以诱导。然而，目前的协议产生的肾脏类器官不成熟且含有脱靶细胞类型。讨论了应用于肾脏肾毒性建模的优点和局限性的有前途的生物工程技术，例如生物打印和“芯片上的肾脏”方法。这篇综述探讨了组织培养中 AKI 的机制和检测，