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29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

Deutsche Hochdruckliga e. V. DHL ® - Deutsche Hypertonie Gesellschaft Deutsches Kompetenzzentrum Bluthochdruck

23. bis 25.11.2005, Berlin

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AT1-Rezeptorblockade verbessert DNA-Schäden in peripheren Blutlymphozyten von Hämodialysepatienten

Meeting Abstract

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  • P. Rutkowski - Medical University of Gdansk (Gdansk, Poland)
  • N.W. Schupp - University of Würzburg (Würzburg, D) )
  • A. Klassen - University of Würzburg (Würzburg, D) )
  • A. Heidland - University of Würzburg (Würzburg, D) )
  • H. Stopper - University of Würzburg (Würzburg, D) )
  • C. Grupp - Center of Internal Medicine, Bamberg )
  • K. Sebekova - Slovak Medical University )

Hypertonie 2005. 29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Berlin, 23.-25.11.2005. Düsseldorf, Köln: German Medical Science; 2006. Doc05hochP50

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/hoch2005/05hoch050.shtml

Published: August 8, 2006

© 2006 Rutkowski 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

In end-stage renal failure (ESRF) genomic damage is enhanced, which may contribute to the development of atherosclerosis and cancer. One important pathway of DNA damage is oxidative stress, which is augmented in ESRF, in part due to RAS stimulation. We hypothesized that the blockade of the AT1 receptor may diminish genomic damage in maintenance hemodialysed (MHD) patients.

Subsequently, 12 MHD patients were treated for 4,5 months with candesartan (4-16mg/daily). DNA damage was measured as micronuclei frequency (MN) in the peripheral blood lymphocytes (PBLs) and estimated thrice before candesartan therapy and afterwards every 6 weeks. Plasma C-reactive protein (CRP), interleukin 6 (IL-6), neopterin, AGE-associated fluorescence (AGE-FL) and advanced oxidative protein products (AOPPs) were additionally analyzed. Seven healthy subjects served as controls.

In comparison with them, MN frequency at baseline was remarkably elevated. After treatment with candesartan the DNA damage was ameliorated significantly. We observed a trend to lowering of AGE-FL and IL-6. AOPPs remained unchanged, while neopterin and CRP increased slightly but not significantly. Systolic and diastolic blood pressure (BP) was lowered. The decline in MN did not correlate with alterations in BP or inflammatory markers.

Our data suggest that blockade of the AT1 receptor with candesartan can reduce DNA damage of PBLs in MHD patients. Its clinical consequences should be further evaluated