Patients with chronic kidney disease (CKD) have signs of genomic instability and, as a consequence, extensive genetic damage, possibly due to accumulation of uraemic toxins, oxidative stress mediators and other endogenous substances with genotoxic properties. We explored factors associated with the presence and background levels of genetic damage in CKD. A cross-sectional study was performed in 91 CKD patients including pre-dialysis (CKD patients; n = 23) and patients undergoing peritoneal dialysis (PD; n = 33) or haemodialysis (HD; n = 35) and with 61 healthy subjects, divided into two subgroups with the older group being in the age range of the patients, serving as controls. Alkaline comet assay and cytokinesis-block micronucleus assay in peripheral blood lymphocytes were used to determine DNA and chromosome damage, respectively, present in CKD. Markers of oxidative stress [malondialdehyde (MDA), advanced glycation end products (AGEs), thiols, advanced oxidation protein products and 8-hydroxy-2′-deoxyguanosine] and markers of inflammation (C-reactive protein, interleukin-6 and tumour necrosis factor alpha) were also measured. Micronucleus (MN) frequency was significantly higher (P < 0.05) in the CKD group (46±4‰) when compared with the older control (oC) group (27.7±14). A significant increase in MN frequency (P < 0.05) was also seen in PD patients (41.9±14‰) versus the oC group. There was no statistically significant difference for the HD group (29.7±15.6‰; P = NS) versus the oC group. Comet assay data showed a significant increase (P < 0.001) of tail DNA intensity in cells of patients with CKD (15.6±7%) with respect to the total control (TC) group (11±1%). PD patients (14.8±7%) also have a significant increase (P < 0.001) versus the TC group. Again, there was no statistically significant difference for the HD group (12.5±3%) compared with the TC group. Patients with MN values in the upper quartile had increased cholesterol, triglycerides, AGEs and MDA levels and lower albumin levels. Multiple logistic regression analysis showed that male gender, diabetes and treatment modality were independently associated with higher levels of DNA damage. Our results suggest that oxidative stress, diabetes, gender and dialysis modality in CKD patients increased DNA and chromosome damage. To confirm these data, prospective clinical trials need to be performed.
There are very few data on analytical biomarker levels in children with congenital heart disease (CHD) before and after cardiopulmonary bypass surgery. We conducted a preliminary study in the Pediatric Hospital of Medical Center IMSS Mexico, to evaluate plasma levels of endothelin-1 (ET-1) and circulating endothelial progenitor cells (CPEC) before and after correction surgery. 56 patients were included: 41 with CHD that required CPB and 15 controls with surgery other than CPB, which were stratified by age (infants, preschool-age-children, and school-age-children). Samples of peripheral blood were taken 24h before and 48h after surgery, cytokine levels (TNF/IL-1β/IL-6/IL-8/IL-10 and IL-12p70) and brachial-artery-flow-mediated dilation (BAFMD) were explored too. Demographic and clinical data were collected. BAFMD was evaluated by-Doppler-ultrasound, the percentage (%) and absolute number (N) of CPEC [CEC and EPC], ET-1 and cytokines concentrations were measured by flow-cytometry, radioimmunoassay and a Bead-Array-cytometric-system, respectively. The% and N of CEC[CD34 + / CD146 + / VEGFR2 + / CD133−] increased in infants versus their control group; and EPC[CD34 + / CD146 + / VEGFR2 + / CD133 +] were higher in the control group of infants versus patients. ET-1 levels were higher in patients than in controls (p = 0.002). N-CEC showed differences between 24 and 48 hours; BAFMD in CPB-preschool at 24H and 48H showed a significant difference. Higher levels of IL-6 and IL-8 were detected in CPB-school-age at 48H. This pilot study observed a significant increase in the levels of CEC and ET-1. To validate these data, subsequent studies should increase the sample size.
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