Kidney Disease

A metabolite that reduces kidney injury

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Science  21 Sep 2018:
Vol. 361, Issue 6408, pp. 1212-1213
DOI: 10.1126/science.361.6408.1212-c

Of critically ill patients, 3 to 10% experience acute kidney injury (AKI), a potentially fatal complication caused by severe metabolic stress arising from restricted blood flow to the kidneys. Currently, there is no specific treatment for AKI. By analyzing urinary metabolites from mice and cardiac surgery patients who developed AKI, Poyan Mehr et al. showed that nicotinamide adenine dinucleotide (NAD+) biogenesis was impaired during AKI. Mice with heterozygous deletion for quinolinate phosphoribosyltransferase, an enzyme involved in NAD+ biogenesis, were more susceptible to AKI. In a phase 1 clinical trial, supplementation of the NAD+-precursor nicotinamide was safe and reduced incidences of AKI in cardiac surgery patients. NAD+ metabolism could be exploited both as a urinary biomarker and as a treatment intervention to reduce incidences of AKI.

Nat. Med. 24, 1351 (2018).

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