IN-DEPTH REVIEWS

Properties Permitting the Renal Cortex to Be the Oxygen Sensor for the Release of Erythropoietin: Clinical Implications

Mitchell L. Halperin ^*1, Surinder Cheema-Dhadli ^*, Shih-Hua Lin , and Kamel S. Kamel ^*

*Division of Nephrology, St. Michael’s Hospital, University of Toronto, Toronto, Ontario, Canada; and Division of Nephrology, Department of Medicine, Tri-Service General Hospital, National Defense National Center, Taipei, Republic of China

¹ To whom correspondence should be addressed. E-mail: mitchell.halperin{at}utoronto.ca.

	Abstract

The Po₂ at this site where erythropoietin release is regulated should vary only when the hemoglobin concentration changes in capillary blood. The kidney cortex is an ideal location for this O₂ sensor for four reasons. First, it extracts a small proportion of the oxygen that is delivered in each liter of blood; this makes the Po₂ signal easier to recognize. Second, there is a constant ratio of the work performed (consumption of O₂) to the renal blood flow rate (delivery of O₂). Third, the high renal blood flow rate improves diffusion of O₂ from capillaries to this O₂ receptor. Fourth, a high renal cortical Pco₂ prevents an additional shift of the O₂:hemoglobin dissociation curve by other factors from being a confounding variable. This suggests that the GFR and the renal blood flow rate should be examined in patients with unexplained anemia or erythrocytosis.