Nicotinamide Attenuates the Progression of Renal Failure in a Mouse Model of Adenine-Induced Chronic Kidney Disease

Nicotinamide adenine dinucleotide (NAD(+)) supplies energy for deoxidation and anti-inflammatory reactions fostering the production of adenosine triphosphate (ATP). The kidney is an essential regulator of body fluids through the excretion of numerous metabolites. Chronic kidney disease (CKD) leads to the accumulation of uremic toxins, which induces chronic inflammation. In this study, the role of NAD(+) in kidney disease was investigated through the supplementation of nicotinamide (Nam), a precursor of NAD(+), to an adenine-induced CKD mouse model. Nam supplementation reduced kidney inflammation and fibrosis and, therefore, prevented the progression of kidney disease. Notably, Nam supplementation also attenuated the accumulation of glycolysis and Krebs cycle metabolites that occurs in renal failure. These effects were due to increased NAD(+) supply, which accelerated NAD(+)-consuming metabolic pathways. Our study suggests that Nam administration may be a novel therapeutic approach for CKD prevention.

Automated summary

NAD(+) plays a crucial role in kidney disease by promoting ATP generation for energy oxidation and anti-inflammatory reactions. Supplementation of the NAD(+) precursor nicotinamide can reduce kidney inflammation and fibrosis, potentially preventing disease progression.