Introduction:

Processes such as mutagenesis, carcinogenesis and teratogenesis are the product of the interaction of agents of endogenous and exogenous origin that interact with the DNA molecule in a chronic way producing ruptures in the double helix, and in complete chromosomes resulting in genomic instability. The oxidative stress to which the cells are subjected when reactive oxygen species (ROS) and reactive nitrogen species (RNS) are formed, which may come from radicals produced as a result of diabetes or in initial stages of chronic kidney disease or in response to inflammatory processes in advanced stages of these pathologies, act as endogenous genotoxic agents.

Objectives:

This research aimed to determine the basal damage in the DNA molecule of hemodialyzed diabetic patients, through the Comet assay, as a bioindicator of genomic instability, during six months of treatment.

Materials and methods:

For this research, a prospective longitudinal cohort study was proposed to compare the different levels of genetic damage before and during the first six of hemodialysis treatment. Baseline damage was evaluated with the comet test or single cell electrophoresis, in venous blood samples from patients diagnosed with Type II Diabetes as a negative control and in diabetic patients with chronic kidney disease before starting dialysis treatment and then during treatment.

Results:

A significant increase in basal and oxidative damage was observed in the genetic material of diabetic patients with chronic kidney disease, compared to negative controls (p< 0.005) and it was also observed that cell damage increases with hemodialysis treatment (p<0.005). The t-Student test was used for independent and paired samples.

Conclusion:

The results obtained in this research allow us to conclude that oxidative stress has a genotoxic effect and that the level of genetic damage is a good bioindicator of the progression of chronic kidney disease and that hemodialysis induces an increase in damage at the level of the genetic material, increasing the risk of carcinogenesis.

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