N-acetylglucosamine ameliorates the transition from acute kidney injury to chronic kidney disease by reducing the accumulation of lipid droplets.

Abstract

Acute kidney injury (AKI) can advance to chronic kidney disease (CKD) and ultimately to renal fibrosis. Inadequate repair of renal tubular epithelial cells (TECs) after injury is a major driver of fibrosis. N-acetylglucosamine (NAG), a natural bioactive monosaccharide involved in metabolism and glycoprotein synthesis, has anti-inflammatory and antioxidant properties. Here, we identify NAG as a key regulator in the transition from AKI to CKD. In a BIRI mouse model, NAG administration reduces renal damage and fibrosis. We show that NAG preserves lysosomal integrity, thereby preventing mitochondrial dysfunction and lipid droplet accumulation. Taken together, these findings suggest that NAG supplementation could be a therapeutic option for managing the AKI-to-CKD transition and other conditions associated with kidney dysfunction.