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Nat Rev Nephrol. 2014 Jul;10(7):415-20. doi: 10.1038/nrneph.2014.76. Epub 2014 May 6.

Hyperosmolarity drives hypertension and CKD--water and salt revisited.

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Division of Nephrology, Eastern Colorado Health Care System, Department of Veteran Affairs, 12700 East 19th Avenue, Room 7015, Aurora, CO 80045, USA.
Universidad del Zulia, Instituto Venezolano de Investigaciones Científicas (IVIC)-Zulia, Maracaibo, Venezuela.
Division of Renal Diseases and Hypertension, University of Colorado, Denver, CO, USA.
Mitsubishi Tanabe-Kyoto (TMK) project, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Department of Nephrology and Mineral Metabolism, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
Program on Work, Environment and Health in Central America (SALTRA), Central American Institute for Studies on Toxic Substances (IRET), Universidad Nacional, Heredia, Costa Rica.
INSERM Unité Mixte de Recherche (UMR)-S 1138/Equipe 2, Centre de Recherche des Cordeliers, Paris, France.
Laboratory of Renal Physiopathology, Intituto Nacional de Cardiología Ignacio Chavez, Mexico City, Mexico.


An epidemic of chronic kidney disease (CKD) in Mesoamerica is providing new insights into the mechanisms by which salt and water might drive hypertension and CKD. Increasingly, evidence suggests that recurrent dehydration and salt loss might be a mechanism that causes CKD, and experimental studies suggest a key role for increased plasma osmolarity in activating both intrarenal (polyol-fructokinase) and extrarenal (vasopressin) pathways that drive renal injury. Thus, we propose that water and salt might influence blood pressure and kidney disease through the timing and combination of their intake, which affect plasma osmolarity as well as intrarenal and extrarenal mechanisms of renal injury. The type of fluid intake might also be important, as fluids containing fructose can trigger activation of these pathways. Future studies should investigate the effects of salt, sugar and fluid intake on plasma osmolarity as a potential pathogenetic mechanism in renal injury and high blood pressure.

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