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Nicotinamide and acute kidney injury
Miguel Fontecha-Barriuso1, Ana M Lopez-Diaz1, Sol Carriazo1
1Laboratory of Experimental Nephrology, Research Institute-Fundacion Jimenez Diaz, Universidad Autonoma de Madrid, 28040 Madrid, Spain.
Clinical Kidney Journal
|December 24, 2021
Summary
Nicotinamide adenine dinucleotide (NAD+) synthesis from tryptophan may be reduced in acute kidney injury (AKI). Supplementation with NAM did not improve kidney function or injury in mice, despite prior suggestions.
Area of Science:
- Biochemistry
- Nephrology
- Metabolic pathways
Background:
- Reduced urine tryptophan and kynurenine in cardiac surgery patients with AKI suggest impaired kynurenine pathway activity.
- Nicotinamide (NAM) supplementation did not restore kidney NAD+ levels or improve outcomes in mouse models of ischemic-reperfusion kidney injury.
- This contrasts with previous studies that did not assess kidney NAD+ levels, filtration, or histology in NAM-treated AKI mice.
Discussion:
- Investigates the therapeutic potential of vitamin B3 vitamers and derivatives (niacin, NAM, NR, NRH, NMN) in kidney injury.
- Explores reasons for conflicting results regarding the efficacy of these compounds in preclinical AKI and chronic kidney disease models.
- Highlights the importance of measuring kidney-specific NAD+ levels and histological outcomes in treatment studies.
Key Insights:
- NAD+ metabolism is altered in AKI, impacting tryptophan-kynurenine pathway activity.
- Direct NAM supplementation may not effectively replete kidney NAD+ or ameliorate AKI.
- Further research is needed to understand the complex role of NAD+ precursors in kidney disease.
Outlook:
- An overview of ongoing clinical trials investigating vitamin B3 derivatives for kidney disease is presented.
- Discusses potential strategies to enhance the efficacy of NAD+ precursor therapies in kidney injury.
- Emphasizes the need for targeted therapeutic approaches based on specific kidney disease mechanisms.
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