Letters| October 13 1999 Membranous Nephropathy Induced by Treatment with Ampiroxicam, a Nonsteroidal Antiinflammatory Drug Subject Area: Nephrology Masataka Nishimura; Masataka Nishimura Division of Nephrology, National Cardiovascular Center, Osaka, Japan Search for other works by this author on: This Site PubMed Google Scholar Takashi Uzu; Takashi Uzu Division of Nephrology, National Cardiovascular Center, Osaka, Japan Search for other works by this author on: This Site PubMed Google Scholar Takashi Inenaga; Takashi Inenaga Division of Nephrology, National Cardiovascular Center, Osaka, Japan Search for other works by this author on: This Site PubMed Google Scholar Genjiro Kimura Genjiro Kimura Division of Nephrology, National Cardiovascular Center, Osaka, Japan Search for other works by this author on: This Site PubMed Google Scholar Nephron (1999) 83 (3): 272–273. https://doi.org/10.1159/000045522 Article history Published Online: October 13 1999 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation Masataka Nishimura, Takashi Uzu, Takashi Inenaga, Genjiro Kimura; Membranous Nephropathy Induced by Treatment with Ampiroxicam, a Nonsteroidal Antiinflammatory Drug. Nephron 1 November 1999; 83 (3): 272–273. https://doi.org/10.1159/000045522 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsNephron Search Advanced Search Article PDF first page preview Close Modal This content is only available via PDF. 1999Copyright / Drug Dosage / DisclaimerCopyright: 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. You do not currently have access to this content.
A case of acute-on-chronic renal failure in a 70-year-old woman with ischemic nephropathy and primary hypothyroidism is presented. Her renal function became progressively worse as the level of serum creatinine increased from 283 to 628 micromol/l (3.2-7.1 mg/dl) within 8 months. Her thyroid function had been normal before the exacerbation of renal failure, but it was markedly reduced with a marked elevation of serum thyroid-stimulating hormone. Thyroid hormone replacement therapy resulted in rapid improvement of the renal function to 159 micromol/l (1.8 mg/dl) of serum creatinine. The development of primary hypothyroidism seemed to worsen the already impaired renal function in this case. We suggest the assessment of thyroid function in patients with unexplained deterioration of renal failure.
Antineutrophil cytoplasmic antibodies (ANCA) are usually diagnostic of pauci-immune crescentic glomerulonephritis. Pauci-immune crescentic glomerulonephritis often has a poor prognosis if not treated aggressively with immunosuppressants. A combination of high doses of corticosteroid and cyclophosphamide has been recommended as an induction therapy. Such therapy is not, however, without severe side-effects. We report a patient with biopsy-documented minimalchange nephropathy associated with a high myeloperoxidase (MPO)-ANCA titre, who responded favourably to moderate doses of oral prednisolone and losartan, an angiotensin II receptor antagonist. This case suggests that the therapy of ANCA-related glomerulonephritis could be adjusted according to the activity of the disease observed on renal histology.
Short-term hypothyroidism has been associated with a reversible rise in serum creatinine levels in patients with normal renal function. A remarkable decline in serum creatinine levels associated with a treatment of severe and prolonged hypothyroidism has rarely been reported so far. We present here 2 patients with chronic renal failure in whom treatment for hypothyroidism resulted in a significant and sustained reduction of their serum creatinine levels. These cases indicate that because hypothyroidism may aggravate the serum creatinine levels, TSH should be considered in screening procedures of patients with chronic renal failure presenting with recent accelerated aggravation of renal function. Hypothyroidism per se, one of its complications or one of its associated autoimmune diseases might play a role in modifying the underlying renal problem.
