Acute Kidney Injury (AKI) is a silent and growing epidemic that has affected over 850 million people worldwide. It is progressing at such an alarming rate that it is projected to become the fifth leading cause of death within a decade. AKI is characterized by disruptions in renal tubular metabolism, leading to decreased or sudden loss of kidney function. Although AKI affects 1 in every 5 individuals worldwide and up to 67% of hospitalized patients, there is no definitive treatment and only minimal supportive care available.Nicotinamide Adenine Dinucleotide (NAD+) is a central molecule which functions as a redox cofactor for several fundamental biochemical processes involved in metabolism and as a co-substrate for signaling enzymes. Notably, AKI is one of the few diseases in humans directly correlated with disrupted NAD+ homeostasis. Previous studies in both human and animal models have shown that renal NAD+ levels decline in ischemic, septic, and chemo toxic AKI. Therefore, I hypothesize that all three NAD+ biosynthetic pathways are suppressed in AKI, with de novo synthesis from the amino acid tryptophan being significantly altered. This alteration results in the accumulation of metabolites that create bottlenecks in the pathway. To answer my hypothesis, we employ a genomic approach through quantitative real-time polymerase chain reaction (qRT-PCR) to measure expression of genes involved in the biosynthesis pathways, particularly the rate-limiting enzymes such as Quinolinic acid phosphoribosyl transferase (QPRT) and Nicotinamide phosphoribosyl transferase (NAMPT) which will provide a mechanistic understanding of how NAD+ metabolism is disrupted during AKI.