gms | German Medical Science

128. Kongress der Deutschen Gesellschaft für Chirurgie

Deutsche Gesellschaft für Chirurgie

03.05. - 06.05.2011, München

Reduction of the Neointimal hyperplasia and calcification in arterialised fistula veins – the effect of vitamin K2 in a CKD/uraemia Rat model

Meeting Abstract

  • Maria Kokozidou - Europäisches Gefäßzentrum Aachen-Maastricht, Klinik für Gefäßchirurgie RWTH Aachen, Aachen
  • Stephan Langer - Europäisches Gefäßzentrum Aachen-Maastricht, Klinik für Gefäßchirurgie RWTH Aachen, Aachen
  • Leon Schurgers - Cardiovascular Research Institute Maastricht, Department of Biochemistry, Maastricht
  • Tina Kessel - Europäisches Gefäßzentrum Aachen-Maastricht, Klinik für Gefäßchirurgie RWTH Aachen, Aachen
  • Jennifer Kranz - Europäisches Gefäßzentrum Aachen-Maastricht, Klinik für Gefäßchirurgie RWTH Aachen, Aachen
  • Michael Jacobs - Europäisches Gefäßzentrum Aachen-Maastricht, Klinik für Gefäßchirurgie RWTH Aachen, Aachen
  • Lieven Kennes - Institute of Medical Statistics, RWTH Aachen, Aachen
  • Karen Arakelyan - Europäisches Gefäßzentrum Aachen-Maastricht, Klinik für Gefäßchirurgie RWTH Aachen, Aachen
  • Thilo Krüger - Department of Nephrology and Clinical Immunology, RWTH Aachen, Aachen
  • Thomas A. Koeppel - Europäisches Gefäßzentrum Aachen-Maastricht, Klinik für Gefäßchirurgie RWTH Aachen, Aachen

Deutsche Gesellschaft für Chirurgie. 128. Kongress der Deutschen Gesellschaft für Chirurgie. München, 03.-06.05.2011. Düsseldorf: German Medical Science GMS Publishing House; 2011. Doc11dgch636

DOI: 10.3205/11dgch636, URN: urn:nbn:de:0183-11dgch6363

Published: May 20, 2011

© 2011 Kokozidou et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.


Outline

Text

Introduction: Neointimal hyperplasia is the main cause of arteriovenous fistula (AVF) failure in chronic kidney disease (CKD) patients while access calcification predicts mortality. Low vitamin K2 intake has been associated with a higher incidence of calcification in the cardiovascular system, through disturbed carboxylation equilibrium of vitamin K-dependent proteins.

Materials and methods: To determine the influence of vitamin K2 we used a rat model that that depicts the influence of CKD in the function of an AVF. The induction of CKD followed an adenine rich diet and the AVFs were micro surgically made in the femoral vessels of the right groin of the rats. The animals were divided in groups fed with normal and adenine rich diet, while two subgroups of the adenine fed animals were either pre fed with food supplemented with vitamin K2 (preventive group), or fed after operation with vitamin K2 (therapeutic group). The animals were sacrificed in days 21, 42 and 63.

Results: There was a significant increase of the neointimal hyperplasia at all time points between the healthy and the CKD animals (p<0.0001) along with a significant shrinking of the media (p<0.0001) and a significant calcification of the venous wall (p<0.0001). The CDK animals that were fed with vitamin K2 presented a significantly lesser neointimal hyperplasia (p<0.0002 for both therapeutic and preventive groups), less shrinking of the media (p<0.0001) compared to the CKD animals without K2 supplement. Significant was the calcification reduction for both therapeutic and preventive groups compared to the non K2 treated CKD animals (p<0.0001).

Conclusion: Vitamin K2 in either a preventive or a therapeutic intake protocol is involved not only in the calcification pathology but also in the neointimal hyperplasia formation making it an even more important therapeutic candidate for dialysis patients.