Disruptions in circadian rhythms contribute to a number of cardiometabolic health risks, including kidney disease. While chronic circadian disruption (CCD) has been recognized as a health risk in a number of other organ systems, we do not understand the effects of CCD on kidney function and sodium handling factors. Individuals with CCDs such as rotating shift workers, have an increased incidence of kidney and cardiovascular disease including impaired sodium excretion patterns. We hypothesized that this impaired sodium excretion is due in part to increased activation of the renin-aldosterone-angiotensin system (RAAS). We recently observed that CCD interrupts blood pressure, heart rate, and activity rhythms. Male 8-week-old C57BL/6J mice were placed under either a normal 12:12 light/dark cycle (control) protocol or a 10:10 light/dark cycle (CCD, T20) protocol, each with ad libitum food and water for 12 weeks. Previous experiments with this model have demonstrated that after 10 weeks the T20 mice did not exhibit a significant difference in mean arterial pressure (MAP) between the light and dark cycles (114±13mmHg during dark cycle, 113±12mmHg during light cycle, p=0.86) as opposed to control animals, who did display a typical circadian pattern in MAP averaging 119±3 mmHg during the dark cycle and 101±2 mmHg during the light cycle (p>0.001). The same pattern persisted in the heart rate (HR) of these animals, with the T20 animals lacking a diurnal variation in HR (537±14 BPM during dark cycle, 526±5 BPM during light cycle, p=0.48), and the control animals maintaining a dark/light period difference (584±11 BPM during dark cycle, 511±4 BPM during light cycle, p=0.001). Prior studies indicate that the circadian timing system controls sodium reabsorption throughout the nephron by effecting aldosterone effects on collecting duct sodium transport systems via the molecular clock. Therefore, aldosterone excretion was assayed in urine from control(n=6) and T20 mice (n=4). Interestingly, T20 animals excreted an order of magnitude more aldosterone than control animals (p<0.015 2-way ANOVA) and lacked a diurnal variation in aldosterone excretion (115.1±51.5 µg/hr during the dark cycle, 64.1±13.1 µg/hr during the light cycle, p=0.17 dark v. light) and during both dark and light phases (0.080±0.014 µg/hr and 0.012±0.003 µg/hr, respectively, p=0.02 dark v. light). T20 mice also lacked a diurnal variation in sodium (UNaV) and potassium (UKV) excretion as compared to control mice. These results suggest that CCD disrupts diurnal sodium handling, at least in part, by disruptions in the RAAS. We further propose that the loss of blood pressure rhythms may be due to hyperaldosteronism in CCD mice.