Strong evidence has demonstrated a link between acute myocardial infarction (MI) and acute kidney injury (AKI). A decrease in cardiac and renal nicotinamide adenine dinucleotide (NAD) has been reported post-cardiac and kidney diseases. The correlation between myocardial and kidney NAD homeostasis in the context of MI-induced AKI (Type-1 CRS) and the potential beneficial impact of NAD boosting therapies in this relatively unexplored disease model are yet to be determined.