急性肾损伤（AKI）是一种严重且高发病率的疾病，但目前仅有支持性治疗方法。尼克酰胺腺嘌呤二核苷酸（NAD +）是三磷酸腺苷（ATP）生成和细胞存活所必需的辅因子。肾脏NAD +生物合成和能量利用的变化是AKI的特征。通过瞄准NAD +作为AKI治疗方法，显示出了很好的应用潜力。然而，追求基于NAD +的治疗需要更深入地了解NAD +生物合成紊乱在AKI中产生的独特驱动因素和影响。本文总结了肾脏在AKI、慢性疾病和衰老中的NAD +生物合成变化。为了增强这种理解，我们还探讨了炎症、怀孕和癌症等会影响NAD +生物合成变化的情景。通过这样做，我们旨在强调不同的NAD +生物合成途径不可互相转换，并提出NAD +的合成方式可能与产生的NAD +同样重要。版权所有 © 2022 Elsevier Inc.。保留所有权利。

Acute kidney injury (AKI) is a serious and highly prevalent disease, yet only supportive treatment is available. Nicotinamide adenine dinucleotide (NAD+) is a cofactor necessary for adenosine triphosphate (ATP) production and cell survival. Changes in renal NAD+ biosynthesis and energy utilization are features of AKI. Targeting NAD+ as an AKI therapy shows promising potential. However, the pursuit of NAD+-based treatments requires deeper understanding of the unique drivers and effects of the NAD+ biosynthesis derangements that arise in AKI. This article summarizes the NAD+ biosynthesis alterations in the kidney in AKI, chronic disease, and aging. To enhance this understanding, we explore instances of NAD+ biosynthesis alterations outside the kidney in inflammation, pregnancy, and cancer. In doing so, we seek to highlight that the different NAD+ biosynthesis pathways are not interconvertible and propose that the way in which NAD+ is synthesized may be just as important as the NAD+ produced.Copyright © 2022 Elsevier Inc. All rights reserved.