The subsequent pathophysiologic mechanisms can be summarized as acute tubular apoptosis, oxidative stress, inflammation, microcirculatory dysfunction, vascular barrier function disorder, local hypoxia, and tissue edema (84)
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These usually include NAD precursors like nicotinamide (NAM), nicotinic acid (NA), nicotinamide riboside (NR), and nicotinamide mononucleotide (NMN)
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