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- W2887579551 abstract "Nicotinamide adenine dinucleotide (NAD+) extends longevity in experimental organisms, raising interest in its impact on human health. De novo NAD+ biosynthesis from tryptophan is evolutionarily conserved yet considered supplanted among higher species by biosynthesis from nicotinamide (NAM). Here we show that a bottleneck enzyme in de novo biosynthesis, quinolinate phosphoribosyltransferase (QPRT), defends renal NAD+ and mediates resistance to acute kidney injury (AKI). Following murine AKI, renal NAD+ fell, quinolinate rose, and QPRT declined. QPRT+/− mice exhibited higher quinolinate, lower NAD+, and higher AKI susceptibility. Metabolomics suggested an elevated urinary quinolinate/tryptophan ratio (uQ/T) as an indicator of reduced QPRT. Elevated uQ/T predicted AKI and other adverse outcomes in critically ill patients. A phase 1 placebo-controlled study of oral NAM demonstrated a dose-related increase in circulating NAD+ metabolites. NAM was well tolerated and was associated with less AKI. Therefore, impaired NAD+ biosynthesis may be a feature of high-risk hospitalizations for which NAD+ augmentation could be beneficial. Impaired NAD+ biosynthesis may be a common feature of high-risk hospitalizations for which NAD+ augmentation could improve therapeutic outcome." @default.
- W2887579551 created "2018-08-22" @default.
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- W2887579551 date "2018-08-20" @default.
- W2887579551 modified "2023-10-17" @default.
- W2887579551 title "De novo NAD+ biosynthetic impairment in acute kidney injury in humans" @default.
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- W2887579551 doi "https://doi.org/10.1038/s41591-018-0138-z" @default.
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