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Genomic Damage in Endstage Renal Disease—Contribution of Uremic Toxins

Patients with end-stage renal disease (ESRD), whether on conservative, peritoneal or hemodialysis therapy, have elevated genomic damage in peripheral blood lymphocytes and an increased cancer incidence, especially of the kidney. The damage is possibly due to accumulation of uremic toxins like advanc...

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Detalles Bibliográficos
Autores principales: Schupp, Nicole, Heidland, August, Stopper, Helga
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3153169/
https://www.ncbi.nlm.nih.gov/pubmed/22069557
http://dx.doi.org/10.3390/toxins2102340
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author Schupp, Nicole
Heidland, August
Stopper, Helga
author_facet Schupp, Nicole
Heidland, August
Stopper, Helga
author_sort Schupp, Nicole
collection PubMed
description Patients with end-stage renal disease (ESRD), whether on conservative, peritoneal or hemodialysis therapy, have elevated genomic damage in peripheral blood lymphocytes and an increased cancer incidence, especially of the kidney. The damage is possibly due to accumulation of uremic toxins like advanced glycation endproducts or homocysteine. However, other endogenous substances with genotoxic properties, which are increased in ESRD, could be involved, such as the blood pressure regulating hormones angiotensin II and aldosterone or the inflammatory cytokine TNF-α. This review provides an overview of genomic damage observed in ESRD patients, focuses on possible underlying causes and shows modulations of the damage by modern dialysis strategies and vitamin supplementation.
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spelling pubmed-31531692011-11-08 Genomic Damage in Endstage Renal Disease—Contribution of Uremic Toxins Schupp, Nicole Heidland, August Stopper, Helga Toxins (Basel) Review Patients with end-stage renal disease (ESRD), whether on conservative, peritoneal or hemodialysis therapy, have elevated genomic damage in peripheral blood lymphocytes and an increased cancer incidence, especially of the kidney. The damage is possibly due to accumulation of uremic toxins like advanced glycation endproducts or homocysteine. However, other endogenous substances with genotoxic properties, which are increased in ESRD, could be involved, such as the blood pressure regulating hormones angiotensin II and aldosterone or the inflammatory cytokine TNF-α. This review provides an overview of genomic damage observed in ESRD patients, focuses on possible underlying causes and shows modulations of the damage by modern dialysis strategies and vitamin supplementation. MDPI 2010-10-11 /pmc/articles/PMC3153169/ /pubmed/22069557 http://dx.doi.org/10.3390/toxins2102340 Text en © 2010 by the authors; licensee MDPI, Basel, Switzerland http://creativecommons.org/licenses/by/3.0/ This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
spellingShingle Review
Schupp, Nicole
Heidland, August
Stopper, Helga
Genomic Damage in Endstage Renal Disease—Contribution of Uremic Toxins
title Genomic Damage in Endstage Renal Disease—Contribution of Uremic Toxins
title_full Genomic Damage in Endstage Renal Disease—Contribution of Uremic Toxins
title_fullStr Genomic Damage in Endstage Renal Disease—Contribution of Uremic Toxins
title_full_unstemmed Genomic Damage in Endstage Renal Disease—Contribution of Uremic Toxins
title_short Genomic Damage in Endstage Renal Disease—Contribution of Uremic Toxins
title_sort genomic damage in endstage renal disease—contribution of uremic toxins
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3153169/
https://www.ncbi.nlm.nih.gov/pubmed/22069557
http://dx.doi.org/10.3390/toxins2102340
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