TY  - JOUR
A1  - Schupp, Nicole
A1  - Heidland, August
A1  - Stopper, Helga
T1  - Genomic Damage in Endstage Renal Disease - Contribution of Uremic Toxins
N2  - 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-. 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 upplementation.
KW  - Toxin
KW  - dialysis
KW  - genotoxicity
KW  - uremic toxins
Y1  - 2010
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-68653
ER  - 
TY  - JOUR
A1  - Schupp, Nicole
A1  - Stopper, Helga
A1  - Heidland, August
T1  - DNA Damage in Chronic Kidney Disease: Evaluation of Clinical Biomarkers
JF  - Oxidative Medicine and Cellular Longevity
N2  - Patients with chronic kidney disease (CKD) exhibit an increased cancer risk compared to a healthy control population. To be able to estimate the cancer risk of the patients and to assess the impact of interventional therapies thereon, it is of particular interest to measure the patients’ burden of genomic damage. Chromosomal abnormalities, reduced DNA repair, and DNA lesions were found indeed in cells of patients with CKD. Biomarkers for DNA damage measurable in easily accessible cells like peripheral blood lymphocytes are chromosomal aberrations, structural DNA lesions, and oxidatively modified DNA bases. In this review the most common methods quantifying the three parameters mentioned above, the cytokinesis-block micronucleus assay, the comet assay, and the quantification of 8-oxo-7,8-dihydro-2′-deoxyguanosine, are evaluated concerning the feasibility of the analysis and regarding the marker’s potential to predict clinical outcomes.
KW  - chronic kidney disease
KW  - cancer risk
KW  - DNA damage
KW  - biomarkers
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-166569
VL  - 2016
IS  - 3592042
ER  -