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      Podocyte Number in the Maturing Rat Kidney

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          Abstract

          Background/Aims: The podocyte is an important cell for maintaining the normal structure and function of the glomerulus. In recent years much attention has been given to the number of podocytes in glomeruli. During this time there has been a debate as to whether podocytes can divide after the capillary-loop stage of development. The aim of this study was to use an unbiased counting method to determine if podocyte number increases after the capillary-loop stage of development. Methods:The fractionator/disector method was used to count podocytes in glomeruli from rats aged 1 day, 5, 12, and 24 weeks. Glomerular volume was also measured with the unbiased Cavalieri principle and used to calculate the density of podocytes per glomerulus. Results: The number of podocytes did not increase from the capillary-loop stage of glomerular development to 24 weeks of age. Glomerular volume increased 3.6-fold during this time, which resulted in a decrease of podocyte density as the rats aged. Conclusion:The study documents that the number of podocytes is stable after the capillary-loop stage of glomerular development. The data does not confirm but adds evidence that podocytes do not divide from the capillary-loop stage of glomerular development to 24 weeks of age in the normal rat.

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          Most cited references18

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          Podocytopenia and disease severity in IgA nephropathy.

          IgA nephropathy is a common form of progressive glomerular disease, associated with proliferation of mesangial cells and mesangial deposition of IgA. The present study was designed to investigate functional and morphological covariates of disease severity in patients with IgA nephropathy. Glomerular hemodynamics, permselectivity and ultrastructure were studied in 17 adult patients with IgA nephropathy using inulin, para-aminohippuric acid (PAH) and 3H-Ficoll clearances and morphometric methods. A mathematical model of macromolecule permeation through a heteroporous membrane was used to characterize glomerular permselectivity. Controls consisted of 14 healthy living kidney donors and 12 healthy volunteers. The patients were heterogeneous in their disease severity, but as a group had a decreased glomerular filtration rate (GFR) and increased urinary protein excretion compared to controls [63 +/- 29 SD vs. 104 +/- 23 mL/min/1.73 m2, P < 0.001, and (median) 1.34 vs. 0.11 g/day, P < 0.0001, respectively). A multivariate analysis of structural and functional relationships revealed GFR depression to be most strongly correlated with the prevalence of global glomerular sclerosis (t = -4.073, P = 0.002). Those patients with the most severe glomerular dysfunction had a reduced number of glomerular visceral epithelial cells (podocytes) per glomerulus. The degree of podocytopenia was related to the extent of glomerular sclerosis and of impairment of permselectivity and GFR, with worsening injury below an apparent threshold podocyte number of about 250 cells per glomerulus. There were no corresponding correlations between these indices of injury and the number of mesangial and endothelial cells. Our findings show that podocyte loss is a concomitant of increasing disease severity in IgA nephropathy. This suggests that podocyte loss may either cause or contribute to the progressive proteinuria, glomerular sclerosis and filtration failure seen in this disorder.
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            POROUS SUBSTRUCTURE OF THE GLOMERULAR SLIT DIAPHRAGM IN THE RAT AND MOUSE

            The highly ordered, isoporous substructure of the glomerular slit diaphragm was revealed in rat and mouse kidneys fixed by perfusion with tannic acid and glutaraldehyde. The slit diaphragm was similar in both animal species and appeared as a continuous junctional band, 300–450 Å wide, consistently present within all slits formed by the epithelial foot processes. The diaphragm exhibited a zipper-like substructure with alternating, periodic cross bridges extending from the podocyte plasma membranes to a central filament which ran parallel to and equidistant from the cell membranes. The dimensions and spacing of the cross bridges defined a uniform population of rectangular pores approximately 40 by 140 Å in cross section and 70 Å in length. The total area of the pores was calculated to be about 2–3% of the total surface area of the glomerular capillaries. Physiological data indicate that the glomerular filter functions as if it were an isoporous membrane which excludes proteins larger than serum albumin. The similarity between the dimensions of the pores in the slit diaphragm and estimates for the size and shape of serum albumin supports the conclusion from tracer experiments that the slit diaphragm may serve as the principal filtration barrier to plasma proteins in the kidney.
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              Accumulation of advanced oxidation protein products induces podocyte apoptosis and deletion through NADPH-dependent mechanisms.

              The accumulation of plasma advanced oxidation protein products (AOPPs) is prevalent in diverse disorders such as diabetes, metabolic syndromes, and chronic kidney disease. To study whether accumulated AOPPs have an important role in the progression of proteinuria and glomerulosclerosis, we chronically treated normal Sprague-Dawley rats with AOPP-modified rat serum albumin. Podocyte apoptosis was significantly increased coincident with the onset of albuminuria and preceded significant losses of glomerular podocytes. Increasing the amount of AOPPs in the media of conditionally immortalized podocytes rapidly triggered the production of intracellular superoxide by activation of NADPH oxidase and this, in turn, led to an upregulation of p53, Bax, caspase 3 activity, and apoptosis. Chronic inhibition of NADPH oxidase by apocynin prevented podocyte apoptosis, ameliorated podocyte depletion, and decreased albuminuria in AOPP-challenged rats. Our study demonstrates that accumulation of AOPPs promotes NADPH oxidase-dependent podocyte depletion by a p53-Bax apoptotic pathway both in vivo and in vitro.
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                Author and article information

                Journal
                AJN
                Am J Nephrol
                10.1159/issn.0250-8095
                American Journal of Nephrology
                S. Karger AG
                0250-8095
                1421-9670
                2011
                January 2011
                22 December 2010
                : 33
                : 1
                : 91-96
                Affiliations
                aDepartment of Pathology, Nanfang Hospital, and bDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, PR China; cMorphometry and Stereology Laboratory, Charles Drew University of Medicine and Science, Los Angeles, Calif., USA
                Author notes
                *John M. Basgen, Morphometry and Stereology Laboratory, Charles R. Drew University of Medicine and Science, 1731 East 120th Street, Los Angeles, CA 90059 (USA), Tel. +1 323 357 3668, Fax +1 323 563 4887, E-Mail johnbasgen@cdrewu.edu
                Article
                322701 PMC3030545 Am J Nephrol 2011;33:91–96
                10.1159/000322701
                PMC3030545
                21196721
                a4deb0fc-185e-41ac-af52-2f9cbd705e0d
                © 2010 S. Karger AG, Basel

                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.

                History
                : 28 August 2010
                : 09 November 2010
                Page count
                Figures: 4, Pages: 6
                Categories
                Original Report: Laboratory Investigation

                Cardiovascular Medicine,Nephrology
                Fractionator/disector,Glomerular volume,Podocyte number,Rat,Stereology

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