Continuous measurement of bladder urine oxygen tension (PO2) is a new method to potentially detect renal medullary hypoxia in patients at risk of acute kidney injury (AKI). To assess its practicality, we developed a computational model of the peristaltic movement of a urine bolus along the ureter and the oxygen exchange between the bolus and ureter wall. This model quantifies the changes in urine PO2 as it transits from the renal pelvis to the bladder. The model parameters were calibrated using experimental data in rabbits, such that most of the model predictions are within ± 1 standard error (SEM) of the reported mean in the experiment, with the average percentage difference being 7.0%. Based on parametric studies performed using a model scaled to the geometric dimensions of a human ureter, we found that bladder-urine PO2 is strongly dependent on the bolus volume (i.e. bolus volume-to-surface area ratio), especially at a volume less than its physiological (baseline) volume (<0.2 ml). For the model assumptions, changes in peristaltic frequency resulted in a minimal change in bladder-urine PO2 (< 1 mmHg). The model also predicted there exists a family of linear relationships of the bladder-urine PO2 and the pelvic-urine PO2 for different input conditions. We conclude that it may technically be possible to predict renal medullary PO2 based on the measurement of bladder-urine PO2, provided there are accurate real-time measurements of model input parameters.