Phosphate and Vitamin D in Chronic Kidney Disease

Description

The enormous progress made during the last decade has resulted in a better conceptual understanding of mineral ion metabolism in general. With regard to chronic kidney disease, the two most affected nutrients are phosphate and vitamin D. This book provides an overview of the physiological aspects of phosphate and vitamin D metabolism, and how their pathological dysregulation facilitates advancement of chronic kidney disease. It looks into the complex molecular and organ cross-talks during disease progression that range from the involvement of fibroblast growth factor (FGF23)-klotho system to impaired phosphate transport to hormonal dysfunctions of PTH and vitamin D. Each chapter clearly presents the clinically and biologically important problems and lists the key unsolved issues related to chronic kidney disease and beyond. Illustrations explaining multi-factorial and multi-organ interactions provide an easy outline for the reader to appreciate the complex biological pathways. For those without prior familiarity with the subject matter, this volume may serve as a quick reference to get updated information on phosphate and vitamin D metabolism.

Informations

• Publié par: S. Karger AG
• Date de parution: 02 mai 2013
• Nombre de lectures: 0
• EAN13: 9783318023701
• Langue: English
• Poids de l'ouvrage: 1 Mo

Extrait

Phosphate and Vitamin D in Chronic Kidney Disease
Contributions to Nephrology
Vol. 180
Series Editor
Claudio Ronco Vicenza
Phosphate and Vitamin D in Chronic Kidney Disease
Volume Editor
Mohammed S. Razzaque Boston, Mass.
25 figures and 4 tables, 2013
Contributions to Nephrology
(Founded 1975 by Geoffrey M. Berlyne)
___________________________
Mohammed S. Razzaque Department of Oral Medicine, Infections & Immunity Harvard School of Dental Medicine 190 Longwood Avenue Research & Education Building, Room 304 Boston, MA 02115 (USA)
Library of Congress Cataloging-in-Publication Data
Phosphate and vitamin D in chronic kidney disease / volume editor, Mohammed S. Razzaque.
p. ; cm. -- (Contributions to nephrology, ISSN 0302-5144 ; vol. 180)
Includes bibliographical references and indexes.
ISBN 978-3-318-02369-5 (hard cover: alk. paper) -- ISBN 978-3-318-02370-1 (e-ISBN)
I. Razzaque, Mohammed S., editor of compilation. II. Series: Contributions to nephrology ; v. 180. 0302-5144
[DNLM: 1. Renal Insufficiency, Chronic--physiopathology. 2. Disease Progression. 3. Phosphates--metabolism. 4. Vitamin D--metabolism. W1 CO778UN v.180 2013 / WJ 342]
RC918.R4
616.6’14--dc23
2013010350
Bibliographic Indices. This publication is listed in bibliographic services, including Current Contents ® and Index Medicus.
Disclaimer. The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publisher and the editor(s). The appearance of advertisements in the book is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.
Drug Dosage. The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any change in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.
© Copyright 2013 by S. Karger AG, P.O. Box, CH-4009 Basel (Switzerland)
www.karger.com
Printed in Germany on acid-free and non-aging paper (ISO 9706) by Bosch Druck, Ergolding
ISSN 0302-5144
e-ISSN 1662-2782
ISBN 978-3-318-02369-5
e-ISBN 978-3-318-02370-1
Contents
Preface
Razzaque, M.S. (Boston, Mass.)
Osteo-Renal Cross-Talk and Phosphate Metabolism by the FGF23-Klotho System
Ohnishi, M.; Razzaque, M.S. (Boston, Mass.)
Extracellular Phosphate as a Signaling Molecule
Michigami, T. (Osaka)
Complex Regulation and Diverse Functions of Alpha-Klotho
Maeda, R.; Imura, A.; Nabeshima, Y. (Kobe)
Klotho and Chronic Kidney Disease
Hu, M.C.; Kuro-o, M.; Moe, O.W. (Dallas, Tex.)
Nuclear Receptor LXR: A New Partner for Sodium-Dependent Phosphate Cotransporters
Caldas, Y. (Aurora, Colo./Zaragoza); Giral, H. (Aurora, Colo.); Sorribas, V. (Zaragoza); Levi, M. (Aurora, Colo.)
Phosphate Toxicity and Vascular Mineralization
Razzaque, M.S. (Boston, Mass./Nagasaki)
Vitamin D and Type II Sodium-Dependent Phosphate Cotransporters
Kido, S.; Kaneko, I.; Tatsumi, S.; Segawa, H.; Miyamoto, K. (Tokushima)
Vitamin D in Chronic Kidney Disease
Li, Y.C. (Chicago, Ill.)
Parathyroid Function in Chronic Kidney Disease: Role of FGF23-Klotho Axis
Koizumi, M.; Komaba, H.; Fukagawa, M. (Isehara)
FGF23-Induced Hypophosphatemia Persists in Hyp Mice Deficient in the WNT Coreceptor Lrp6
Uchihashi, K.; Nakatani, T. (Boston, Mass.); Goetz, R.; Mohammadi, M. (New York, N.Y.); He, X.; Razzaque, M.S. (Boston, Mass.)
Can Salivary Phosphate Levels Be an Early Biomarker to Monitor the Evolvement of Obesity?
Hartman, M.-L. (Cambridge, Mass.); Groppo, F. (Piracicaba, SP); Ohnishi, M. (Boston, Mass.); Goodson, J.M.; Hasturk, H.; Tavares, M.; Yaskell, T.; Floros, C. (Cambridge, Mass.); Behbehani, K. (Dasman); Razzaque, M.S. (Boston, Mass.)
Author Index
Subject Index
Preface
The common thread connecting the chapters of this book is the two most affected nutrients in chronic kidney disease - phosphate and vitamin D. Chapters are committed to provide the physiological aspects of phosphate and vitamin D metabolism, and how their pathological dysregulation facilitates the advancement of chronic kidney disease and influences the eventual outcome of the patients. I selected the chapters to present a framework of what the readers would be able to follow to understand the complex molecular and organ cross-talks during disease progression, ranging from the involvement of the fibroblast growth factor 23-klotho system in impaired phosphate transport to parathyroid dysfunction. Each chapter clearly presents the clinically important problems and lists the key unsolved issues related to chronic kidney disease. Readers will be able to use this simple book as a quick reference for updated information on phosphate and vitamin D metabolism without prior acquaintance with the field. My time and efforts of writing, editing and organizing this book will prove worthwhile if its contents inspire young physicians and scientists to take on the challenge of solving some of these clinically imperative issues, through their dynamic thinking and innovative research works. Finally, I would like to express my thanks to the research scientists in my laboratory at the Harvard School of Dental Medicine in Boston who, through their hard work, generated an enormous amount of clinically and biologically meaningful data on phosphate and vitamin D metabolism in the shortest possible time. Lastly, this project would not have reached its present form without the help and continued encouragement from the Razzaque family members (Rafi, Yuki, Newaz, Zahid, Shahed, Lisa, Muhit and Nilufar Begum).
Mohammed S. Razzaque , Boston, Mass.
Razzaque MS (ed): Phosphate and Vitamin D in Chronic Kidney Disease. Contrib Nephrol. Basel, Karger, 2013, vol 180, pp 1-13 (DOI: 10.1159/000346774)
______________________
Osteo-Renal Cross-Talk and Phosphate Metabolism by the FGF23-Klotho System
Mutsuko Ohnishi Mohammed S. Razzaque
Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, Mass., USA
______________________
Abstract
Phosphate is widely distributed in the body and an adequate balance is required for maintaining essential cellular and organ functions. Dysregulation of phosphate balance, either in the form of hypophosphatemia or hyperphosphatemia can induce disorders ranging from rickets/osteomalacia to cardiovascular calcification. A physiologic phosphate balance is delicately maintained by multiorgan cross-talks among the intestine, kidney, and bone. Sodium-dependent phosphate (Na/Pi) cotransporters present in the intestine and kidney play a major role in phosphate absorption and reabsorption, according to the body’s demand. Some of the calcium regulating factors, including parathyroid hormone and vitamin D can influence the activities of Na/Pi cotransporters, and thereby can affect phosphate balance. In addition, molecular analysis of the unexplained hypophosphatemic diseases, including autosomal-dominant hypophosphatemic rickets and tumor-induced osteomalacia has led to the identification of fibroblast growth factor 23 (FGF23). Subsequent studies have documented that bone-derived FGF23 and kidney-derived klotho can form an endocrine network to control urinary phosphate excretion. Studies have also documented negative effect of FGF23/klotho system on vitamin D metabolism and Na/Pi cotransporter activities. This article will summarize how the FGF23/klotho system might influence systemic phosphate metabolism, and consequences of its abnormal regulation will be briefly described.
Copyright © 2013 S. Karger AG, Basel
Adequate phosphate balance is essential for the maintenance of fundamental cellular functions of the mammalian system, ranging from energy metabolism to mineral ion metabolism [ 1 ] . Despite such important biological functions, the molecular regulation of phosphate metabolism is not clearly understood. One of the reasons for such a lack of understanding of phosphate metabolism lies in the fact that it was often considered to be a secondary process, and controlled by the calcium regulating factors, such as parathyroid hormone (PTH) and vitamin D. However, molecular analysis of certain hypophosphatemic and hyperphos-phatemic diseases has established a calcium-independent active regulation of phosphate metabolism [ 2 - 6 ] .
Phosphate is a widely distributed element in the body, with bone and teeth consuming more than 80% of total phosphate where it is stored as apatite. Various soft tissues, including skeletal muscle utilize remaining phosphate, while less than 0.1% of phosphate is present within the cells and in the extracellular fluids [