Urinary PO2 as a biomarker for medullary hypoxia

Abstract

Despite receiving ~25% of the cardiac output, the mammalian kidney is susceptible to hypoxia, owing in part to the large difference of blood and O2 supply between the cortex and the medulla. As a result, when renal O2 supply is reduced, e.g., during cardiac surgery performed under cardiopulmonary bypass (CPB), acute kidney injury (AKI) may result. The objective of this study is to assess whether urinary PO2 is an effective biomarker for medullary hypoxia and for predicting the development of AKI following CPB. To do so, we have developed a detailed mathematical model that simulates autoregulation, solute transport and oxygenation in the rat kidney. The model predicts the distribution of PO2, which exhibits substantial variations along and perpendicular to the corticomedullary axis, throughout the kidney and ureter. We simulate kidney function and medullary oxygenation during CPB and tested the hypothesis that urinary PO2 may be a biomarker for AKI risk in hospital setting. This research was supported in part by NIH grant DK-89066, and NSF grant DBI-1300426.