A case of non-secretory multiple myeloma presenting as primary plasma cell leukaemia in a 65 year old woman is presented. Bone pain was the initial clinical manifestation. Laboratory analysis showed 20% of circulating immature plasma cells. Despite the presence of osteolytic lesions, no M-component could be demonstrated in serum protein electrophoresis, and serum and urine immunoelectrophoresis. Bone marrow aspirate demonstrated an 83% infiltration of plasma cells showing various degrees of immaturity. Immunofluorescence with monoclonal antisera demonstrated intracytoplasmic kappa light chains in a high percentage of plasma cells. Immature plasma cells without cellular capacity to synthesize and excrete complete immunoglobulins could be more aggressive, leading to an initial leukaemic process. Previous work regarding possible pathogenetic mechanisms, clinical and laboratory features, and response to treatment of this extremely rare association are reviewed.
Letters| December 11 2008 Intravenous Fe-Gluconate-Na for Iron-Deficient Patients on Hemodialysis Subject Area: Nephrology Julio Pascual; Julio Pascual aServicios deNefrología y Search for other works by this author on: This Site PubMed Google Scholar José L. Teruel; José L. Teruel aServicios deNefrología y Search for other works by this author on: This Site PubMed Google Scholar Fernando Liaño; Fernando Liaño aServicios deNefrología y Search for other works by this author on: This Site PubMed Google Scholar Anna Sureda; Anna Sureda bHematología, Hospital Ramón y Cajal, Madrid, España Search for other works by this author on: This Site PubMed Google Scholar Joaquín Ortuño Joaquín Ortuño aServicios deNefrología y Search for other works by this author on: This Site PubMed Google Scholar Nephron (1992) 60 (1): 121. https://doi.org/10.1159/000186721 Article history Published Online: December 11 2008 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 Julio Pascual, José L. Teruel, Fernando Liaño, Anna Sureda, Joaquín Ortuño; Intravenous Fe-Gluconate-Na for Iron-Deficient Patients on Hemodialysis. Nephron 1 January 1992; 60 (1): 121. https://doi.org/10.1159/000186721 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. 1992Copyright / 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.
Journal Article Serious adverse reactions after intravenous ferric gluconate Get access J. Pascual, J. Pascual Departments of Nephrology and Haematology Hospital Ramόn y Cajal28034 Madrid, Spain Search for other works by this author on: Oxford Academic PubMed Google Scholar J. L. Teruel, J. L. Teruel Departments of Nephrology and Haematology Hospital Ramόn y Cajal28034 Madrid, Spain Search for other works by this author on: Oxford Academic PubMed Google Scholar F. Liaño, F. Liaño Departments of Nephrology and Haematology Hospital Ramόn y Cajal28034 Madrid, Spain Search for other works by this author on: Oxford Academic PubMed Google Scholar A. Sureda, A. Sureda Departments of Nephrology and Haematology Hospital Ramόn y Cajal28034 Madrid, Spain Search for other works by this author on: Oxford Academic PubMed Google Scholar J. Ortuño J. Ortuño Departments of Nephrology and Haematology Hospital Ramόn y Cajal28034 Madrid, Spain Search for other works by this author on: Oxford Academic PubMed Google Scholar Nephrology Dialysis Transplantation, Volume 7, Issue 3, 1992, Pages 271–272, https://doi.org/10.1093/oxfordjournals.ndt.a092122 Published: 01 January 1992
Impaired renal production of erythropoietin (EPO) is the main cause of the blunted marrow response to the anemia in end-stage renal disease (ESRD) [1]. Recombinant human EPO (rHuEPO) is being widely used to correct the anemia due to ESRD [2]. Several studies have documented an increase not only in the peripheral progenitor cells burst- (BFU-E) and colony-forming units—erythroid (CFU-E) during treatment with rHuEPO [3–6] but also in CFU—granulocyte, macrophage (CFU-GM) [4, 6], CFU—megakaryocyte (CFU-Mk) [4], and the multipotent hematopoietic stem cells CFU—granulocyte, erythrocyte, megakaryocyte, macrophage (CFU-GEMM) [5, 6]. These studies are based on in vitro culture systems, poorly standardized among different laboratories because of their complex nature and not very useful in clinical practice because of the 2-week wait necessary before results are available.
Hereditary hemorrhagic telangiectasia (HHT) is an inherited disorder characterized by the presence of generalized mucocutaneous and visceral telangiectasias associated with recurrent bleeding. In order to analyze the mechanism of bleeding in HHT we studied the hemostatic system and platelet in vitro aggregation in 7 unrelated patients suffering from HHT. Unlike the authors of previous reports, we could not find any significant alteration of the parameters measured suggesting a possible local role of the affected endothelial cells.
Jose A. Lorente, C/Monforte de Lemos 83,12-C, E-28029 Madrid (Spain) Dear Sir, The maintenance of an access site to the circulatory system is one of the determinants of the survival and well-being of patients on hemodialysis. Thrombosis of the fistula can occur either soon after surgery or as a late event. Early thrombosis is usually due to technical problems. Several approaches have been used to deal with late thrombosis: surgery, using a Fogarty balloon catheter; percutaneous transluminal angioplasty (PTA), and local fibrinolysis. We report our experience with systemic fi-brinolysis in a case of early endogenous arteriovenous fistula (AVF) thrombosis. To our knowledge, systemic fibrinolysis has not been reported as a successful therapeutic alternative for this condition. . The patient, a 36-year-old man diagnosed as having chronic renal failure of unknown etiology 6 years earlier, was admitted because of impaired renal function. Dialytic treatment was indicated and an internal AVF was performed on the right forearm. The next day, he felt dizzy after getting up, and 2 h later a nonfunctional AVF was diagnosed. After treatment by open Fogarty balloon thrombectomy, thrill was still not present and a Doppler examination did not detect blood flow. After a bolus injection of 210,000 IU, a systemic peripheral venous infusion of 4,000IU/kg/h of uroki-nase was started. Three hours later, he felt pressure on the AVF site, and a thrill was present 5 h after fibrinolytic treatment was started. Urokinase was administered for a total of 8 h and then full-dose heparin was infused for 24 h. Fifteen days later, the AVF was used for hemodialysis, and it is still patent 6 months after the procedure. Thrombosis is the most frequent cause of fistula failure. Despite all efforts to treat this complication, including correction of technical problems during the preceding surgery and thrombectomy, fistula salvage is frequently impossible. Two nonsurgical methods are available for restoring the pantency of thrombosed dialysis grafts: thrombolysis and/or PTA. These methods make the graft immediately available for dialysis, as opposed to the several days that may be required after placement of a new graft, and tend to prolong the life of each graft. PTA without the administration of a fibrinolytic agent has been used with varying success rates [1–4]. The 6-month patency rate varies between 68 and 76% [2, 5]. Fibrinolytic therapy has been used in problems similar to that of our patient, such as thrombosed hemodialysis catheters [6] and synthetic graft thrombosis [7]. Mixed results have been reported
Three cases of spontaneous peritonitis caused by Enterococcus faecium are presented. The underlying condition was alcoholic cirrhosis in each case. This enterococcal species has never before been reported as a cause of spontaneous bacterial peritonitis. Two patients responded to therapy. The development of enterococcal peritonitis and the cases documented in the literature are briefly reviewed. Taxonomic problems with pathogenic, clinical, and therapeutic implications are discussed.
A case of acute lymphoblastic leukemia (ALL) in a 16-year-old male with a 47,XYY karyotype is reported. This chromosome aneuploidy was found in both bone marrow (BM) cells and mitogen-stimulated lymphocytes. Immunologic profile of leukemic cells showed a null phenotype. To our knowledge, this is the fifth case reported in the literature.