Macromolecules and Urolithiasis: Parallels and Paradoxes

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Abstract

Long-standing interest in the possible role of macromolecules in urolithiasis stems from the observation that all human kidney stones consist of a complex amalgam of mineral and organic material. This review summarises what is currently known or is hypothesised about the influences of urinary macromolecules, especially proteins, on the formation of calcium oxalate crystals, their attachment to renal epithelial cells, and their subsequent destruction within those cells. Although a list is provided of proteins that have either been detected in stones or have been implicated by virtue of their effects on crystallization, only a select handful, which have been intensively studied, have been singled out for individual discussion. The review ends with a speculative discussion of the applicability of current knowledge to the investigation and treatment of urolithiasis.

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Innovative materials processing strategies: a biomimetic approach.

A H Heuer, D J Fink, V Laraia … (1992)

Many organisms construct structural ceramic (biomineral) composites from seemingly mundane materials; cell-mediated processes control both the nucleation and growth of mineral and the development of composite microarchitecture. Living systems fabricate biocomposites by: (i) confining biomineralization within specific subunit compartments; (ii) producing a specific mineral with defined crystal size and orientation; and (iii) packaging many incremental units together in a moving front process to form fully densified, macroscopic structures. By adapting biological principles, materials scientists are attempting to produce novel materials. To date, neither the elegance of the biomineral assembly mechanisms nor the intricate composite microarchitectures have been duplicated by nonbiological processing. However, substantial progress has been made in the understanding of how biomineralization occurs, and the first steps are now being taken to exploit the basic principles involved.

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Calcium oxalate nephrolithiasis: effect of renal crystal deposition on the cellular composition of the renal interstitium.

E Boeve, C Noordermeer, F. G. Schröder … (1999)

Urinary calcium oxalate (CaOx) crystals and crystal agglomerates are normally harmlessly excreted, but in nephrolithiasis they are retained by tubular epithelial cells and shifted into the renal interstitium. This crystalline material induces an inflammatory response consisting of an increase in the number of interstitial cells and an expansion of the extracellular matrix. The newly arrived cells either derive from the blood or the connective tissue or they are formed by local proliferation. Identification of the cells that surround the interstitial crystals is a first step in investigating the question of whether the interstitial cells could remove the crystalline material. Therefore, we performed an immunohistochemical study on the kidneys of rats made hyperoxaluric by ethylene glycol (EG) and ammonium chloride (AC). Attention was paid to expression of the leukocyte common antigen (LCA), which identifies all types of leukocytes, the ED1 antigen, which is specific for monocytes and macrophages, and the major histocompatibility class II antigen (MHC II), which is present on dendritic cells, B lymphocytes, and activated macrophages. The results obtained were compared with those seen in two human kidney specimens with acute and chronic oxalosis. In both rat and humans, macrophages and multinucleated giant cells are the major cells that encapsulate the interstitial crystals. This similarity in response underlines the relevance of the rat nephrolithiasis model. The rat experiments showed, furthermore, that the number of interstitial crystals and the amount of biochemically measured kidney-associated oxalate both decrease with time, if the nephrolithiatic agents EG and AC are omitted from the drinking water. Further studies must clarify whether macrophages and multinucleated giant cells are able to remove the interstitial crystals and how these cells are recruited at the inflammatory site.

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Cell-Crystal Interactions and Kidney Stone Formation

JohnC. Lieske, Sergio Deganello, F.Gary Toback (1998)

Background: Renal tubular fluid in the distal nephron is supersaturated with calcium and oxalate ions that nucleate to form crystals of calcium oxalate monohydrate (COM), the most common crystal in renal stones. How these nascent crystals are retained in the nephron to form calculi in certain individuals is not known. Methods: The results of experiments conducted in this and other laboratories that employ cell culture model systems to explore renal epithelial cell-urinary crystal interactions are described. Results: COM crystals rapidly adhere to anionic sites on the surface of cultured renal epithelial cells, but this process can be inhibited, if specific urinary anions such as glycosaminoglycans, uropontin, nephrocalcin, or citrate are available to coat the crystalline surface. Therefore, competition for the crystal surface between soluble anions in tubular fluid and anions on the apical cell surface could determine whether or not a crystal binds to the cell. A similar paradigm describes adhesion of calcium phosphate (hydroxyapatite) crystals, also a common constituent of human stones. Once bound, COM and hydroxyapatite crystals are quickly internalized by renal cells; reorganization of the cytoskeleton, alterations in gene expression, and initiation of proliferation may then ensue. Each of these cellular events appears to be regulated by a different set of extracellular factors. Over several weeks in culture, renal cells (BSC-1 line) dissolve internalized crystals, although once a cell binds a crystal, additional crystals are more likely to bind, possibly forming a positive feedback loop that results in kidney stone formation. Conclusions: Increased knowledge about the cell-crystal interaction, including identification of molecules in tubular fluid and on the cell surface that modulate the process, and understanding its mechanism of action appear critical for explaining the pathogenesis of nephrolithiasis.

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Author and article information

Journal

Journal ID (publisher-id): NEP

Journal ID (nlm-ta): Nephron Physiol

Journal ID (doi): 10.1159/issn.1660-2137

Title: Nephron Physiology

Publisher: S. Karger AG

ISBN: 978-3-8055-7852-3

ISBN: 978-3-318-06156-7

ISSN (Electronic): 1660-2137

Publication date Subscription-year: 2004

Publication date (Print): October 2004

Publication date (Electronic): 19 October 2004

Volume: 98

Issue: 2

Pages: p37-p42

Affiliations

Department of Surgery, Flinders University School of Medicine, Flinders Medical Centre, Adelaide, Australia

Article

Publisher ID: 80262 Other ID: Nephron Physiol 2004;98:p37–p42

DOI: 10.1159/000080262

PubMed ID: 15499213

SO-VID: cbb3221f-f60e-4dc5-a861-02a7545587f4

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Copyright: 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. 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 changes 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. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication 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.

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Macromolecules and Urolithiasis: Parallels and Paradoxes

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Abstract

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Karger: Nephrology

Most cited references 15

Innovative materials processing strategies: a biomimetic approach.

Calcium oxalate nephrolithiasis: effect of renal crystal deposition on the cellular composition of the renal interstitium.

Cell-Crystal Interactions and Kidney Stone Formation

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