Understanding the molecular shifts that occur as Acinetobacter baumannii transitions from peak log phase to the death phase is crucial for unraveling its survival mechanisms under physiological stress. As A. baumannii progresses from log to late stationary phase, it faces increasing oxidative stress, toxic byproducts, and resource depletion that challenge its survival. This study investigates transcriptomic changes during this transition, focusing on adaptive strategies employed under these harsh conditions. Growth curve analysis revealed that 4 h post-inoculation (HPI) corresponds to peak log phase, while 8 HPI marks the end of stationary phase and the transition into the death phase. Transcriptomic analysis identified 907 differentially expressed genes (DEGs) between 4 and 8 HPI, with 421 upregulated and 486 downregulated at 8HPI. Gene Ontology (GO) analysis of downregulated genes revealed significant suppression of several transport-related systems, notably NADH-ubiquinone oxidoreductase and F₀F₁ ATP synthase. This pattern suggests a cellular shift toward reduced energy production during the stationary phase. Translation-related genes, such as ribosomal proteins, were also broadly downregulated, indicating a global reduction in biosynthetic activity. Conversely, metabolic reprogramming at 8 HPI was marked by upregulation of pathways involved in alternative carbon utilization, including the tricarballylate utilization (tcu) and malonate decarboxylase (mdc) operons. ICP-MS analysis of intracellular ion quantification revealed increased levels of Fe, Mg, Zn, Cu, Ca, and K at 8 HPI. Although not statistically significant, this trend suggests ion accumulation driven by enhanced transport activity during the logarithmic growth phase. By identifying these adaptive responses, this study enhances understanding of A. baumanniis survival strategies under stress and may inform therapeutic interventions targeting metabolic vulnerabilities during infection.