NDT Advance Access originally published online on August 12, 2009
Nephrology Dialysis Transplantation 2009 24(11):3282-3283; doi:10.1093/ndt/gfp399
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© The Author 2009. Published by Oxford University Press [on behalf of ERA-EDTA]. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org
Salt is getting under our skin*
Department of Nephrology, Leiden University Medical Center, Albinusdreef 2, PO Box 9600, 2300 RC, Leiden, The Netherlands
Correspondence and offprint requests to: Ton J. Rabelink; E-mail: t.rabelink@lumc.nl
Keywords: hypertension; interstitium; myeloid cells; sodium retention; VEGF
| The first 10% of the full text of this article appears below. |
Traditionally, the Na+ cation is thought to be largely restricted to the extracellular compartment, while K+ is stored intracellularly. This balance is maintained by the activity of the Na/K-ATPase sodium pump in the cell membrane. As Na+ and its accompanying anions are the principal extracellular osmoles, extracellular accumulation of Na+ inevitably also leads to fluid retention and expansion of the extracellular volume (ECV). In Guytonian physiology, Na+ balance and its regulation by the kidney are predominant determinants of blood volume and thus of blood pressure. In recent years, however, new insight has been shed into this classical physiological paradigm.
Carefully performed balance studies had already indicated that substantial Na+ retention might occur, without the expected fluid retention and weight gain [1]. The