Nicotinamide Riboside Restores NAD+ and Improves Mitochondrial Function in HIV-Nephropathy: Preclinical Findings

Synopsis

HIV disease remains prevalent in the United States and especially in sub-Saharan Africa. In mice with HIV-associated kidney disease (HIVAN), their kidney cells showed mitochondrial dysfunction. Researchers suspected that low levels of NAD+, a key energy molecule, might contribute to kidney damage. They treated HIVAN mice with nicotinamide riboside (NR), a NAD+ precursor, or INT-747, a drug that activates FXR. Both treatments improved kidney function and reduced tubular injury. Analysis of kidney tissue showed that HIVAN mice had low NAD+ levels and reduced activity of enzymes important for energy production, like NAMPT and Sirtuin3. Restoring NAD+ levels improved these problems. These findings suggest that NAD+ deficiency drives kidney damage in HIVAN and that boosting NAD+ could be a potential treatment.

Journal

American Journal of Physiology-Renal Physiology