Abstract
Disturbances in kidney tubular cell metabolism are increasingly recognized as a feature of acute kidney injury (AKI). In AKI, tubular epithelial cells undergo abnormal metabolic shifts that notably disrupt NAD(+) metabolism. Recent advancements have highlighted the critical role of NAD(+) metabolism in AKI, revealing that acute disruptions may lead to lasting cellular changes, thereby promoting the transition to chronic kidney disease (CKD). This review explores the molecular mechanisms underlying metabolic dysfunction in AKI, with a focus on NAD(+) metabolism, and proposes several cellular processes through which acute aberrations in NAD(+) may contribute to long-term changes in the kidney.