+1 Recommend
1 collections
      • Record: found
      • Abstract: found
      • Article: found

      Dimensions of Arteriovenous Fistulas in Patients with Autosomal Dominant Polycystic Kidney Disease

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          Background/Aim: Aneurysms are known manifestations of autosomal dominant polycystic kidney disease (ADPKD). We investigated whether the dimensions of arteriovenous fistulas created for performance of haemodialysis were affected by the original disease. Methods: The lumen diameter of the fistula was studied by ultrasound in 19 patients with ADPKD and in 19 control patients. The patients’ sex, age, the duration of their fistulas, haemoglobin values and blood pressure levels were similar in both groups. The monitoring was performed along the forearm part of the vein, and the maximal diameter was measured. The diameters at the two needle insertion sites were also measured. Results: The ADPKD patients had a significantly higher fistula diameter than the control patients: 12 (range 8–19) mm versus 8 (range 6–24) mm at the widest level (p = 0.003). There were no significant differences in the diameters at the needle insertion sites. Conclusion: The receiving veins of arteriovenous fistulas in patients with ADPKD have an abnormality that causes a greater than normal dilatation in response to the arterialization. We postulate that this phenomenon is linked with the increased prevalence of aneurysms in ADPKD.

          Related collections

          Most cited references 2

          • Record: found
          • Abstract: not found
          • Article: not found

          Autosomal dominant polycystic kidney disease.

           Aaron Gabow (1993)
            • Record: found
            • Abstract: found
            • Article: not found

            Cellular localization and tissue distribution of polycystin-1.

             L Spruit,  J. Bruijn,  E Heer (1999)
            Autosomal dominant polycystic kidney disease (ADPKD) is characterized by the formation of fluid-filled cysts in both kidneys, in addition to a variety of extra-renal manifestations. The PKD1 gene product, polycystin-1, encodes a novel protein with a putative role in cell-cell/cell-matrix interactions. The present study we focused on the (sub)cellular localization of polycystin-1 in cultured cells, and on its tissue distribution in various organs. In Madin Darby canine kidney (MDCK) cells, several polyclonal antibodies showed intense staining at the sites of interaction between adjacent cells, which remained after Triton extraction. Weak cytoplasmic staining was observed. No signal was detected at the free borders of cell aggregates, supporting a role for polycystin-1 in cell-cell interactions. At the tissue level, polycystin-1 expression was observed in specific cell types in tissues with known manifestations of the disease, but also in tissues of organs which have not been reported to be affected in ADPKD. Expression was frequently seen in epithelia, but also in endocrine cells (pancreatic islets, parathyroid-producing cells, clusters in the adenohypophysis, clusters in the adrenal gland, and Leydig cells in the testis). In addition, expression was observed in myocardium and more weakly in myocytes of cardiac valves, of the cerebral arteries, and of skeletal muscles. Copyright 1999 John Wiley & Sons, Ltd.

              Author and article information

              S. Karger AG
              May 2000
              21 April 2000
              : 85
              : 1
              : 50-53
              aDepartment of Nephrology and bTransplant Unit, Sahlgrenska University Hospital, Göteborg, and cDepartment of Radiology, Höglandssjukhuset, Eksjö, Sweden
              45629 Nephron 2000;85:50–53
              © 2000 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: 12, Pages: 4
              Self URI (application/pdf):
              Original Paper


              Comment on this article