Linking genetic damage with chronic kidney disease

Over 500 million people worldwide are affected by chronic kidney disease (CKD), and 12 million people die prematurely each year of heart disease associated with CKD. Patients suffering from CKD generally show signs of extensive genetic damage, possibly due to the accumulation of endogenous toxins and oxidative stress mediators. In a recently published study, Rangel-López and coworkers from various Mexican Medical Research Units explored factors associated with the presence of genetic damage in CKD. The extent of DNA and chromosome damage was measured with the help of a cytokinesis-block micronucleus assay and a comet assay. Using Enzo’s ELISA kits, levels of the oxidative stress marker, 8-hydroxy-2′-deoxyguanosine (8-OHdG), and the inflammation markers, interleukin-6 (IL-6) and tumour necrosis factor alpha (TNF-α), were also evaluated in the sera of healthy subjects, pre-dialysis CKD patients, and CKD patients undergoing either peritoneal dialysis (PD) or haemodialysis (HD). Micronucleus (MN) frequency and 8-OHdG levels were found to be significantly higher in pre-dialysis CKD patients as well as in patients treated with PD. IL-6 and TNF-α were also increased in pre-dialysis CKD patients with the highest levels found in patients undergoing HD. Finally, a significant increase of tail DNA intensity was observed by comet assay in the cells of pre-dialysis and PD-treated CKD patients. In contrast, patients treated with HD did not show increased MN frequency, 8-OHdG levels or tail DNA intensity.
These interesting findings suggest that oxidative stress, inflammation and dialysis modality could play a critical role in the pathology of chronic kidney disease by increasing DNA and chromosome damage.

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