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      Cyclophosphamide Pulse Therapy in Advanced Progressive IgA Nephropathy

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          Abstract

          For advanced progressive primary IgA nephropathy (IgAN) no established therapy exists. We conducted a prospective, uncontrolled trial to evaluate the effect of intravenous cyclophosphamide pulse (CyP) therapy on the course of advanced progressive IgAN. Twenty-one patients (mean age 52 ± 10 years; male/female 20/1) with biopsy-proven IgAN without crescentic extracapillary proliferation and a serum creatinine of more than 2.0 mg/dl and/or an increase more than 25% in the previous 3 months were included. Patients were treated with CyP (750 mg/m<sup>2 </sup>body surface area) every 4 weeks for 6 months and low dose oral prednisolone. The loss of renal function per year was significantly reduced from 16% before therapy to 4% after therapy (p < 0.001). A further increase >25% of serum creatinine after therapy was observed in 8 patients after 0.7 years (range 0.3–3.0 years), and 3 of these patients developed end-stage renal disease. Proteinuria decreased significantly during CyP therapy. A low nadir of white blood cell and platelet count was associated with a better renal outcome (p = 0.025). In conclusion, CyP therapy and low dose oral prednisolone is effective in preserving renal function in a subgroup of patients with advanced progressive IgAN.

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          Most cited references 3

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          Renoprotective properties of ACE-inhibition in non-diabetic nephropathies with non-nephrotic proteinuria.

          Stratum 2 of the Ramipril Efficacy in Nephropathy (REIN) study has already shown that in patients with chronic nephropathies and proteinuria of 3 g or more per 24 h, angiotensin-converting enzyme (ACE) inhibition reduced the rate of decline in glomerular filtration and halved the combined risk of doubling of serum creatinine or end-stage renal failure (ESRF) found in controls on placebo plus conventional antihypertensives. In REIN stratum 1, reported here, 24 h proteinuria was 1 g or more but less than 3 g per 24 h. In stratum 1 of this double-blind trial 186 patients were randomised to a ramipril or a control (placebo plus conventional antihypertensive therapy) group targeted at achieving a diastolic blood pressure of less than 90 mm Hg. The primary endpoints were change in glomerular filtration rate (GFR) and time to ESRF or overt proteinuria (> or =53 g/24 h). Median follow-up was 31 months. The decline in GFR per month was not significantly different (ramipril 0.26 [SE 0.05] mL per min per 1.73m2, control 0.29 [0.06]). Progression to ESRF was significantly less common in the ramipril group (9/99 vs 18/87) for a relative risk (RR) of 2.72 (95% CI 1.22-6.08); so was progression to overt proteinuria (15/99 vs 27/87, RR 2.40 [1.27-4.52]). Patients with a baseline GFR of 45 mL/min/1.73 m2 or less and proteinuria of 1.5 g/24 h or more had more rapid progression and gained the most from ramipril treatment. Proteinuria decreased by 13% in the ramipril group and increased by 15% in the controls. Cardiovascular events were similar. As expected, the rate of decline in GFR and the frequency of ESRF were much lower in stratum 1 than they had been in stratum 2. In non-diabetic nephropathies, ACE inhibition confers renoprotection even to patients with non-nephrotic proteinuria.
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            Corticosteroids in IgA nephropathy: a randomised controlled trial

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              Controlled trial of pulse methylprednisolone versus two regimens of pulse cyclophosphamide in severe lupus nephritis

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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
                2003
                April 2003
                17 November 2004
                : 93
                : 4
                : c131-c136
                Affiliations
                Division of Nephrology, Department of Internal Medicine II, University of Ulm, Ulm, Germany
                Article
                70232 Nephron Clin Pract 2003;93:c131–c136
                10.1159/000070232
                12759581
                © 2003 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: 1, References: 21, Pages: 1
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/70232
                Categories
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