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      Long-Term Evaluation of Neuromyopathy in Live Donor FMF Amyloidotic Kidney Transplant Recipients

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          Background: Neuromyopathy was reported to be a problem among live donor familial Mediterranean fever (FMF) amyloid kidney transplant recipients. We aimed to address this issue on a long-term basis. Methods: 14 FMF amyloid live donor kidney transplant recipients with a mean post-transplant follow-up period of 82.43 ± 50.1 months in comparison to a control group of 19 non-amyloid renal transplant patients were subjected to thorough neurological examination, laboratory and electrophysiologic studies. Results: Both groups were comparable with regard to mean serum creatinine levels cyclosporine doses (p > 0.05), however trough cyclosporine levels were significantly lower in the amyloidotics than the controls (p = 0.04). Serum creatine phosphokinase was comparable in both groups (p = 0.59). The amyloid patients showed significantly increased polyphasic motor unit potentials and abnormal interference patterns in the biceps brachii muscle (p = 0.03) and the abductor polices brevis muscle (p = 0.05). Multivariate analysis showed a significant level for biceps myopathy in amyloidotics (p = 0.001). Both groups attained no difference with regard to median nerve conduction velocity. Conclusion: Electrophysiologically evidenced neuromyopathy is more liable to occur in long-term live donor FMF amyloidotic kidney transplant recipients than in the other non-amyloidotic kidney transplant recipients even with no clinical manifestations or high creatine phosphokinase levels.

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          Most cited references 10

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          Colchicine myopathy and neuropathy.

          Although colchicine has been used for centuries, its neuromuscular toxicity in humans is largely unrecognized. In this report we describe a characteristic syndrome of myopathy and neuropathy and present 12 new cases of the condition. Colchicine myopathy may occur in patients with gout who take customary doses of the drug but who have elevated plasma drug levels because of altered renal function. It usually presents with proximal weakness and always presents with elevation of serum creatine kinase; both features remit within three to four weeks after the drug is discontinued. The accompanying axonal polyneuropathy is mild and resolves slowly. Electromyography of proximal muscles shows a myopathy that is marked by abnormal spontaneous activity. Because of these features, colchicine myoneuropathy is usually misdiagnosed initially, either as probable polymyositis or as uremic neuropathy. The myopathy is vacuolar, marked by accumulation of lysosomes and autophagic vacuoles unrelated to necrosis or to the mild denervation in distal muscles. The morphologic changes in muscle suggest that the pathogenesis involves disruption of a microtubule-dependent cytoskeletal network that interacts with lysosomes. Correct diagnosis may save patients with this disorder from inappropriate therapy.
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            Acute onset of colchicine myoneuropathy in cardiac transplant recipients: case studies of three patients

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              Long-term outcome of live donor kidney transplantation for renal amyloidosis


                Author and article information

                Am J Nephrol
                American Journal of Nephrology
                S. Karger AG
                December 2004
                28 February 2005
                : 24
                : 6
                : 582-586
                aNephrology Unit, Mansoura Urology and Nephrology Center, and bNeurology Department, Mansoura University, Mansoura, Egypt
                82251 Am J Nephrol 2004;24:582–586
                © 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
                Tables: 5, References: 16, Pages: 5
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/82251
                Original Report: Laboratory Investigation

                Cardiovascular Medicine, Nephrology

                Amyloidosis, Neuromyopathy, Kidney transplantation


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