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      Acute and Transient Podocyte Loss and Proteinuria in Preeclampsia

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          Abstract

          Glomerular podocytes are known to regulate proteinuria and podocyturia correlated with proteinuria. Podocyturia, the urinary excretion of viable podocytes (glomerular epithelial cells), has been associated with proteinuria in preeclampsia. This study is the first to investigate the time course alterations of podocyturia in patients with preeclampsia (11 cases) and normotensive pregnant women (45 cases). Urinalysis was performed at 35 weeks of gestation, 4 days after delivery, and 1 month after delivery. In patients with preeclampsia, podocyturia was evident at 35 weeks of gestation and 4 days after delivery, while proteinuria had already decreased at 4 days after delivery. At 1 month after delivery, almost no patients exhibited podocyturia. In control cases, proteinuria was not significant throughout the study period. However, 9 of the 45 controls exhibited transient and mild podocyturia at 4 days after delivery without proteinuria or hypertension. Statistics indicated a correlation between urinary podocyte number and blood pressure, but not with proteinuria. In conclusion, podocyturia in preeclampsia is transient and almost synchronous with heavy proteinuria. The results suggest that acute podocyte loss implicates podocyturia as the possible mechanism of proteinuria in women with preeclampsia.

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          Preeclampsia and the risk of end-stage renal disease.

          Torbjørn Leivestad, Bo B. Iversen, Rolv Skjærven … (2008)
          It is unknown whether preeclampsia is a risk marker for subsequent end-stage renal disease (ESRD). We linked data from the Medical Birth Registry of Norway, which contains data on all births in Norway since 1967, with data from the Norwegian Renal Registry, which contains data on all patients receiving a diagnosis of end-stage renal disease (ESRD) since 1980, to assess the association between preeclampsia in one or more pregnancies and the subsequent development of ESRD. The study population consisted of women who had had a first singleton birth between 1967 and 1991; we included data from up to three pregnancies. ESRD developed in 477 of 570,433 women a mean (+/-SD) of 17+/-9 years after the first pregnancy (overall rate, 3.7 per 100,000 women per year). Among women who had been pregnant one or more times, preeclampsia during the first pregnancy was associated with a relative risk of ESRD of 4.7 (95% confidence interval [CI], 3.6 to 6.1). Among women who had been pregnant two or more times, preeclampsia during the first pregnancy was associated with a relative risk of ESRD of 3.2 (95% CI, 2.2 to 4.9), preeclampsia during the second pregnancy with a relative risk of 6.7 (95% CI, 4.3 to 10.6), and preeclampsia during both pregnancies with a relative risk of 6.4 (95% CI, 3.0 to 13.5). Among women who had been pregnant three or more times, preeclampsia during one pregnancy was associated with a relative risk of ESRD of 6.3 (95% CI, 4.1 to 9.9), and preeclampsia during two or three pregnancies was associated with a relative risk of 15.5 (95% CI, 7.8 to 30.8). Having a low-birth-weight or preterm infant increased the relative risk of ESRD. The results were similar after adjustment for possible confounders and after exclusion of women who had kidney disease, rheumatic disease, essential hypertension, or diabetes mellitus before pregnancy. Although the absolute risk of ESRD in women who have had preeclampsia is low, preeclampsia is a marker for an increased risk of subsequent ESRD. 2008 Massachusetts Medical Society
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            Podocyte depletion and glomerulosclerosis have a direct relationship in the PAN-treated rat.

            Kathryn J Wiggins, Sagar Goyal, Nathaniel Holzman … (2001)
            Podocytes are highly differentiated glomerular epithelial cells with limited potential to divide. They are responsible for maintaining and supporting the glomerular basement membrane so as to facilitate efficient filtration. The hypothesis tested was whether the development of glomerulosclerosis in the puromycin aminonucleoside (PAN)-treated rat could be attributed to podocyte depletion. PAN was injected in Sprague-Dawley rats once, twice, or three times at 30-day intervals. Podocytes were counted in glomeruli using immunoperoxidase histochemistry and antibodies to both GLEPP1 (PTPRO) and WT-1. Podocytes were assayed in urine using reverse transcription-quantitative polymerase chain reaction (RT-QPCR). Glomerular areas were measured by computerized morphometry. In a preliminary experiment, a single injection of PAN caused a reduction in the glomerular podocyte count by 25%. Additional independent confirmation that podocytes were lost from glomeruli after PAN injection was obtained identifying detached podocytes in Bowman's space, measurement of nephrin and GLEPP1 mRNAs in urine, ultrastructural analysis of glomeruli, and identification of TUNEL-positive apoptotic podocytes in glomeruli. In a second experiment, sequential podocyte depletion by 15, 31, and 53% was achieved by the administration of one, two, or three injections of PAN at 30-day intervals. The region of the glomerulus devoid of podocytes developed glomerulosclerosis, and this area progressively increased as podocytes were progressively depleted. The correlation coefficient (r(2)) value for the relationship between percent podocyte depletion and glomerulosclerotic area was 0.99. The Y intercept of this plot showed that glomerulosclerosis was initiated when only 10 to 20% of podocytes were lost. This report supports the growing body of data linking glomerulosclerosis directly to a reduction in relative podocyte number [increased glomerular area per podocyte (GAPP)]. It raises important questions related to the mechanisms of podocyte loss, strategies for prevention of podocyte depletion, and the prevention of progression of glomerular diseases.
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              Urinary excretion of podocytes in patients with diabetic nephropathy.

              I Ebihara, Taishi Nakamura, N. Shimada … (2000)
              Detection of podocytes in the urinary sediments of children with glomerulonephritis has been shown to indicate severe injury to the podocytes. The aim of the present study was to determine whether podocytes are present in the urine sediments of adult patients with diabetes with and without nephropathy and whether trandolapril is effective for podocyte injury. Fifty diabetic patients (10 with normoalbuminuria, 15 with microalbuminuria, 15 with macroalbuminuria and 10 with chronic renal failure) and 10 healthy controls were studied. Urinary podocytes were examined by immunofluorescence using monoclonal antibodies against podocalyxin, which is present on the surface of podocytes. In addition, we studied plasma metalloproteinase (MMP)-9 concentrations in all patients. Urinary podocytes were absent in healthy controls, diabetic patients with normoalbuminuria and diabetic patients with chronic renal failure. Podocytes were detected in the urine of eight diabetic patients with microalbuminuria (53%) and of 12 patients with macroalbuminuria (80%). The number of podocytes in the urine of patients with macroalbuminuria was significantly greater than in patients with microalbuminuria (P:<0.01). However, there was no relationship between urinary albumin excretion and urinary podocytes. In addition, plasma MMP-9 concentrations were significantly correlated with the number of urinary podocytes (P:<0.01). Twelve diabetic patients with macroalbuminuria and eight patients with microalbuminuria who had urinary podocytes were treated with the angiotensin-converting enzyme inhibitor trandolapril. Urinary albumin excretion, the number of podocytes and plasma MMP-9 concentrations were reduced by the trandolapril treatment. Podocytes in the urine may be a useful marker of disease activity in diabetic nephropathy. Trandolapril may be effective for podocyte injury.
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                Author and article information

                Journal
                Journal ID (publisher-id): NEC
                Journal ID (nlm-ta): Nephron Clin Pract
                Journal ID (doi): 10.1159/issn.1660-2110
                Title: Nephron Clinical Practice
                Publisher: S. Karger AG
                ISSN (Electronic): 1660-2110
                Publication date Subscription-year: 2009
                Publication date (Print): May 2009
                Publication date (Electronic): 18 April 2009
                Volume: 112
                Issue: 2
                Pages: c65-c70
                Affiliations
                aMolecular Pathology and bObstetrics and Gynecology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Ibaraki, and cDepartment of Pediatrics, Yoshida Hospital, Niigata, Japan
                Article
                Publisher ID: 213083 Other ID: Nephron Clin Pract 2009;112:c65–c70
                DOI: 10.1159/000213083
                PubMed ID: 19390204
                SO-VID: b62d204b-ac37-4605-b4e4-c4f687a7dcbf
                Copyright © © 2009 S. Karger AG, Basel
                License:

                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
                Date received : 31 July 2008
                Date accepted : 16 October 2008
                Page count
                Figures: 2, Tables: 3, References: 18, Pages: 1
                Categories
                Subject: Original Paper

                ScienceOpen disciplines: Cardiovascular Medicine,Nephrology
                Keywords: Proteinuria,Podocyturia,Preeclampsia,Glomerular endothelial cells
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine, Nephrology
                Keywords: Proteinuria, Podocyturia, Preeclampsia, Glomerular endothelial cells

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