NAD+ preservation is increasingly being recognized as a way of delaying the effects of ageing on health and thus potentially extend lifetime. The kidney is a crucial organ in de novo NAD+ biosynthesis. In acute kidney injury and chronic kidney disease, de novo NAD+ biosynthesis is impaired, and substantial decreases in the levels of NAD+ can reduce energy generation. More recently, NAD+ augmentation through supplementation with nicotinamide mononucleotide (NMN) or nicotinamide (NAM), an NAD+ precursor, has been proposed as for the prevention of numerous kidney illnesses, including AKI, CKD, the AKI-to-CKD transition, and diabetic nephropathy. Our experimental results showed that NAD+ lowered TGF-β1-induced extracellular matrix deposition in kidney organoids produced from hiPSCs, confirming its therapeutic efficacy in CKD....In conclusion, activation of Insig1 in PTCs markedly attenuated CKD, possibly by maintaining NAD+ homeostasis and controlling ER expansion via the transcriptional repression of Aldh1a1 in PTCs.