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

Mitchell L. Halperin^*, 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

Address correspondence to: Dr. Mitchell L. Halperin, Department of Medicine, University of Toronto, St. Michael’s Hospital Annex, Lab #1, Research Wing, 38 Shuter Street, Toronto, Ontario, M5B 1A6, Canada. Phone: 416-864-5292; Fax: 416-864-5943; mitchell.halperin{at}utoronto.ca

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.

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				R. G. Evans, B. S. Gardiner, D. W. Smith, and P. M. O'Connor Intrarenal oxygenation: unique challenges and the biophysical basis of homeostasis Am J Physiol Renal Physiol, November 1, 2008; 295(5): F1259 - F1270. [Abstract] [Full Text] [PDF]