To understand how arterial-to-venous (AV) oxygen shunting influences kidney oxygenation, a mathematical model of oxygen transport in the renal cortex was created. The model consists of a multiscale hierarchy of eleven counter-current systems representing the various branch levels of the cortical vasculature. At each level equations describing the reactive-advection-diffusion of oxygen are solved. Factors critical in renal oxygen transport incorporated into the model include: the parallel geometry of arteries and veins and their respective sizes, variation of blood velocity in each vessel, oxygen transport (along the vessels, between the vessels and between vessel and parenchyma), non-linear binding of oxygen to hemoglobin and the consumption of oxygen by renal tissue. The model is calibrated using published measurements of cortical vascular geometry and microvascular PO2. The model predicts that AV oxygen shunting is quantitatively significant, and estimates how much kidney oxygen consumption must change, in face of altered renal blood flow, to maintain cortical tissue PO2 at a stable level. It is demonstrated that oxygen shunting increases as renal oxygen consumption or arterial PO2 increases. Oxygen shunting also increases as renal blood flow is reduced within the physiological range or during mild hemodilution. In severe ischemia or anemia, or when kidney oxygen consumption increases, AV oxygen shunting in proximal vascular elements may reduce the oxygen content of blood destined for the medullary circulation, thereby exacerbating the development of tissue hypoxia. That is, cortical ischemia could cause medullary hypoxia even when medullary perfusion is maintained. Cortical AV oxygen shunting limits the change in oxygen delivery to cortical tissue and stabilizes tissue PO2 when arterial PO2 changes, but renders the cortex and perhaps also the medulla susceptible to hypoxia when oxygen delivery falls or consumption increases.