Literature DB >> 21195917

Salivary glands: a new player in phosphorus metabolism.

Vincenzo Savica1, Lorenzo A Calò, Domenico Santoro, Paolo Monardo, Giuseppe Santoro, Ugo Muraca, Paul A Davis, Guido Bellinghieri.   

Abstract

In uremic patients, hyperphosphatemia is associated with cardiovascular calcification and increased cardiovascular mortality. Despite the use of phosphate binders and dietary phosphate limitation in addition to dialysis, only 50% of dialysis patients achieve recommended serum phosphate levels. The identification of other approaches for serum phosphorus reduction is therefore necessary. We have approached this issue by taking into account the relationships between serum phosphate, kidney function, and saliva. Saliva was chosen because the anatomy and/or physiology of acini, the secretive units of salivary glands, shares similarities with that of the renal tubules. Salivary fluid contains electrolytes including phosphate that, when related with the amount of salivary secretion per day, raises the interest in identifying another possible approach for phosphorus removal in uremic patients. This article reports studies from our laboratory in the last 3 to 4 years, which have demonstrated a hyperphosphoric salivary content in patients with chronic renal failure and those with end-stage renal disease under chronic dialysis that, in patients with chronic renal failure, linearly correlates with serum phosphate in patients with chronic renal failure and negatively with GFR. The ingestion of the saliva and later its absorption in the intestinal tract starts a vicious circle between salivary phosphate secretion and fasting phosphate absorption, thereby worsening hyperphosphatemia. Therefore, salivary phosphate binding could be a useful approach to serum phosphate level reduction in dialysis patients. The reduction of salivary phosphate with the salivary phosphate binder, chitosan-loaded chewing gum, chewed during fasting periods, as an add-on to phosphate binders could lead to a better control of hyperphosphatemia, as demonstrated in our study, which confirms the importance of this approach.
Copyright © 2011 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.

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Year:  2011        PMID: 21195917     DOI: 10.1053/j.jrn.2010.11.007

Source DB:  PubMed          Journal:  J Ren Nutr        ISSN: 1051-2276            Impact factor:   3.655


  7 in total

Review 1.  Control of phosphate balance by the kidney and intestine.

Authors:  Ichiro Kaneko; Sawako Tatsumi; Hiroko Segawa; Ken-Ichi Miyamoto
Journal:  Clin Exp Nephrol       Date:  2016-11-30       Impact factor: 2.801

Review 2.  Vascular calcification: When should we interfere in chronic kidney disease patients and how?

Authors:  Usama Abdel Azim Sharaf El Din; Mona Mansour Salem; Dina Ossama Abdulazim
Journal:  World J Nephrol       Date:  2016-09-06

3.  Systemic network for dietary inorganic phosphate adaptation among three organs.

Authors:  Kayo Ikuta; Hiroko Segawa; Ai Hanazaki; Toru Fujii; Ichiro Kaneko; Yuji Shiozaki; Sawako Tatsumi; Yasuko Ishikawa; Ken-Ichi Miyamoto
Journal:  Pflugers Arch       Date:  2018-12-06       Impact factor: 3.657

4.  Taste genetics and gastrointestinal symptoms experienced in chronic kidney disease.

Authors:  K J Manley
Journal:  Eur J Clin Nutr       Date:  2015-05-27       Impact factor: 4.016

5.  Phosphorus and nutrition in chronic kidney disease.

Authors:  Emilio González-Parra; Carolina Gracia-Iguacel; Jesús Egido; Alberto Ortiz
Journal:  Int J Nephrol       Date:  2012-05-30

Review 6.  Hyperphosphatemia. The hidden killer in chronic kidney disease.

Authors:  Akram M Askar
Journal:  Saudi Med J       Date:  2015-01       Impact factor: 1.484

Review 7.  Phosphate control in dialysis.

Authors:  Adamasco Cupisti; Maurizio Gallieni; Maria Antonietta Rizzo; Stefania Caria; Mario Meola; Piergiorgio Bolasco
Journal:  Int J Nephrol Renovasc Dis       Date:  2013-10-04
  7 in total

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