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Nicotinamide and acute kidney injury

2021; Oxford University Press; Volume: 14; Issue: 12 Linguagem: Inglês

10.1093/ckj/sfab173

2048-8513

Miguel Fontecha‐Barriuso, Ana M. López-Diaz, Sol Carriazo, Alberto Ortíz, Ana B. Sanz,

Calcium signaling and nucleotide metabolism

ABSTRACT In a recent issue of ckj, Piedrafita et al. reported that urine tryptophan and kynurenine are reduced in cardiac bypass surgery patients that develop acute kidney injury (AKI), suggesting reduced activity of the kynurenine pathway of nicotinamide (NAM) adenine dinucleotide (NAD+) synthesis from tryptophan. However, NAM supplementation aiming at repleting NAD+ did not replete kidney NAD+ and did not improve glomerular filtration or reduce histological injury in ischaemic–reperfusion kidney injury in mice. The lack of improvement of kidney injury is partially at odds with prior reports that did not study kidney NAD+, glomerular filtration or histology in NAM-treated wild-type mice with AKI. We now present an overview of research on therapy with vitamin B3 vitamers and derivate molecules {niacin, Nicotinamide [NAM; niacinamide], NAM riboside [Nicotinamide riboside (NR)], Reduced nicotinamide riboside [NRH] and NAM mononucleotide} in kidney injury, including an overview of ongoing clinical trials, and discuss the potential explanations for diverging reports on the impact of these therapeutic approaches on pre-clinical acute and chronic kidney disease.