De novo NAD+ biosynthetic impairment in acute kidney injury in humans View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-08-20

AUTHORS

Ali Poyan Mehr, Mei T. Tran, Kenneth M. Ralto, David E. Leaf, Vaughan Washco, Joseph Messmer, Adam Lerner, Ajay Kher, Steven H. Kim, Charbel C. Khoury, Shoshana J. Herzig, Mary E. Trovato, Noemie Simon-Tillaux, Matthew R. Lynch, Ravi I. Thadhani, Clary B. Clish, Kamal R. Khabbaz, Eugene P. Rhee, Sushrut S. Waikar, Anders H. Berg, Samir M. Parikh

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. More... »

PAGES

1351-1359

Journal

TITLE

Nature Medicine

ISSUE

9

VOLUME

24

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41591-018-0138-z

DOI

http://dx.doi.org/10.1038/s41591-018-0138-z

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1106133484

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30127395


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