Determination of genotoxic effects in hemodialysis patients with chronic kidney disease and the role of diabetes mellitus and other biochemical parameters.

Determination of genotoxic effects in hemodialysis patients with chronic kidney disease and the role of diabetes mellitus and other biochemical parameters.

Mamur, Sevcan;Yuzbasioglu, Deniz;Altok, Kadriye;Unal, Fatma;Deger, Serpil Muge;
mutation research 2019 Vol. 844 pp. 46-53
333
mamur2019determinationmutation

Abstract

Chronic kidney disease (CKD) is a common health problem. The primary etiology of CKD is diabetes mellitus (DM). The aim of our study is to determine the possible role of DM and also effects of other factors such as hypertension, duration of hemodialysis (HD), age, sex, body mass index (BMI), and levels of hemoglobin (HB), intact parathormone (iPTH), and ferritin on genetic alterations in maintenance HD patients using chromosomal aberrations (CAs), sister chromatid exchanges (SCEs), and micronucleus (MN) tests. According to the results, the frequency of CAs (p = 0.001), SCEs (p < 0.001) and MN (p < 0.001) statistically increased in HD patients compared to controls. However, there was no significant effect of diabetes as well as other factors on CA, SCE (except at factor of age), and MN in HD patients compared to controls. The mitotic (MI), replication (RI) and nuclear division indices (NDI) significantly decreased in HD patients compared to controls (p < 0.001). In addition, RI (p < 0.001) and NDI (p = 0.047) were significantly decreased in diabetic HD patients than the non-diabetic HD patients. There was no relation between the frequency of CA, SCE and MN and duration of HD treatment with correlation analysis. According to univariate regression analyses, only having CKD was significantly associated with the values of CA, SCE and MN. However, in multivariate analyses, only having CKD remained as significantly associated with CA, SCE and MN values. Consequently, the clastogenic and mutagenic effects increased in HD patients compared to controls; unlike DM in which cell proliferation decreased.

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