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Published ahead of print on June 28, 2007
J Am Soc Nephrol 18: 2278-2280, 2007
© 2007 American Society of Nephrology
doi: 10.1681/ASN.2006121416
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Science in Renal Medicine

A Brain Protein–Centered View of H+ Buffering

Manjula Gowrishankar*, Kamel S. Kamel{dagger} and Mitchell L. Halperin{dagger}

* Division of Pediatric Nephrology, Stollery Children's Hospital, University of Alberta, Edmonton, Alberta, and {dagger} Division of Nephrology, St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada

Correspondence: 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; E-mail: mitchell.halperin{at}utoronto.ca

In the traditional approach to buffering of H+ during metabolic acidosis, the sole focus is on lowering the H+ concentration, but this overlooks several important points. First, increased binding of H+ to proteins changes their charge, shape, and possibly function. Second, organs in which buffering of H+ occurs is not assessed even though it would be advantageous to spare brain proteins in this process. Third, only the arterial and not the capillary PCO2 of individual organs is considered. This article provides a "brain protein–centered" view, which leads to different conclusions concerning the way H+ are removed physiologically.


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M. Gowrishankar, A.P.C.P. Carlotti, C. St George-Hyslop, D. Bohn, K.S. Kamel, M.R. Davids, and M.L. Halperin
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