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      Urinary Excretion of Vascular Endothelial Growth Factor Is Increased in Children with Reflux Nephropathy

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          Abstract

          Background: We determined the urinary levels of vascular endothelial growth factor (VEGF) in patients with reflux nephropathy to elucidate its clinical significance as a predictor of the development of renal damage. Patients and Methods: Seventy-two patients (47 boys and 25 girls) aged 10–18 years with reflux nephropathy were studied. Vesicoureteral reflux was resolved surgically in all cases at least 2 years before enrollment. Urinary VEGF, α<sub>1</sub>-microglobulin and albumin levels were determined using morning spot urine samples. Plasma VEGF, serum creatinine and β<sub>2</sub>-microglobulin levels were measured simultaneously. The severity of renal scarring and right and left kidney function were assessed by <sup>99m</sup>Tc dimercaptosuccinic acid renal scan. Results: No significant correlation was found between the plasma and urinary VEGF levels. Urinary VEGF increased significantly with the increase in severity of renal scarring (p < 0.0001). Urinary VEGF levels correlated significantly with serum β<sub>2</sub>-microglobulin (p < 0.002) and urinary α<sub>1</sub>-microglobulin (p < 0.03). No significant correlation of urinary VEGF levels with serum creatinine and urinary albumin levels was found. Nearly 60% of the patients with elevated urinary VEGF had normal levels of serum β<sub>2</sub>-microglobulin and/or urinary α<sub>1</sub>-miocroglobulin. Conclusions: Urinary VEGF level appears to reflect its production in the kidney. Since urinary VEGF shows a propensity to elevate before the increase in serum β<sub>2</sub>-microglobulin and/or urinary α<sub>1</sub>-microglobulin, urinary VEGF may serve as an early indicator of the development of reflux nephropathy.

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          Most cited references 16

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          A role for uric acid in the progression of renal disease.

          Hyperuricemia is associated with renal disease, but it is usually considered a marker of renal dysfunction rather than a risk factor for progression. Recent studies have reported that mild hyperuricemia in normal rats induced by the uricase inhibitor, oxonic acid (OA), results in hypertension, intrarenal vascular disease, and renal injury. This led to the hypothesis that uric acid may contribute to progressive renal disease. To examine the effect of hyperuricemia on renal disease progression, rats were fed 2% OA for 6 wk after 5/6 remnant kidney (RK) surgery with or without the xanthine oxidase inhibitor, allopurinol, or the uricosuric agent, benziodarone. Renal function and histologic studies were performed at 6 wk. Given observations that uric acid induces vascular disease, the effect of uric acid on vascular smooth muscle cells in culture was also examined. RK rats developed transient hyperuricemia (2.7 mg/dl at week 2), but then levels returned to baseline by week 6 (1.4 mg/dl). In contrast, RK+OA rats developed higher and more persistent hyperuricemia (6 wk, 3.2 mg/dl). Hyperuricemic rats demonstrated higher BP, greater proteinuria, and higher serum creatinine than RK rats. Hyperuricemic RK rats had more renal hypertrophy and greater glomerulosclerosis (24.2 +/- 2.5 versus 17.5 +/- 3.4%; P < 0.05) and interstitial fibrosis (1.89 +/- 0.45 versus 1.52 +/- 0.47; P < 0.05). Hyperuricemic rats developed vascular disease consisting of thickening of the preglomerular arteries with smooth muscle cell proliferation; these changes were significantly more severe than a historical RK group with similar BP. Allopurinol significantly reduced uric acid levels and blocked the renal functional and histologic changes. Benziodarone reduced uric acid levels less effectively and only partially improved BP and renal function, with minimal effect on the vascular changes. To better understand the mechanism for the vascular disease, the expression of COX-2 and renin were examined. Hyperuricemic rats showed increased renal renin and COX-2 expression, the latter especially in preglomerular arterial vessels. In in vitro studies, cultured vascular smooth muscle cells incubated with uric acid also generated COX-2 with time-dependent proliferation, which was prevented by either a COX-2 or TXA-2 receptor inhibitor. Hyperuricemia accelerates renal progression in the RK model via a mechanism linked to high systemic BP and COX-2-mediated, thromboxane-induced vascular disease. These studies provide direct evidence that uric acid may be a true mediator of renal disease and progression.
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            Comparing Stroke Incidence Worldwide : What Makes Studies Comparable?

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              Vascular permeability factor mRNA and protein expression in human kidney.

              Vascular permeability factor (VPF), also known as vascular endothelial growth factor (VEGF), is a potent microvascular permeability-enhancing mediator as well as a selective mitogen for vascular endothelium. In this study, in situ hybridization and immunohistochemistry co-localized VPF mRNA and protein to glomerular visceral epithelial cells in human kidneys. Northern analysis confirmed the presence of VPF mRNA of expected size. The finding of VPF in renal glomerular epithelium identifies a potent mediator of permeability and endothelial proliferation whose role in renal physiology and pathology requires investigation.
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                Author and article information

                Journal
                NEC
                Nephron Clin Pract
                10.1159/issn.1660-2110
                Nephron Clinical Practice
                S. Karger AG
                1660-2110
                2004
                November 2004
                17 November 2004
                : 98
                : 3
                : c73-c78
                Affiliations
                aDepartment of Urology, Iwate Medical University School of Medicine, Morioka, and Departments of bNephrology, Endocrinology and Hypertension, and cUrology, Tohoku University School of Medicine, Sendai, Japan
                Article
                80676 Nephron Clin Pract 2004;98:c73–c78
                10.1159/000080676
                15528940
                © 2004 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.

                Page count
                Figures: 2, Tables: 2, References: 22, Pages: 1
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/80676
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