Y. A. Saienko^1,2*, D. S. Krasnenkov¹, K. K. Midlovets¹, V. V. Korcheva¹,
Y. E. Rebrova^1,3, D. D. Yepishyna¹, B. M. Mankovsky¹

¹SI “D.F. Chebotarev Institute of Gerontology, National Academy
of Medical Sciences of Ukraine”, Kyiv;
²SI “Center for Cardiology and Cardiac Surgery
of the Ministry of Health of Ukraine”, Kyiv
³P.L. Shupyk National University of Health Care of Ukraine, Kyiv;
*e-mail: ysaenko1981@gmail.com

Received: 04 April 2025; Revised: 23 April 2025;
Accepted: 25 April 2025; Available on-line: 12 May 2025

Chronic kidney disease (CKD) as one of the most common complications of type 2 diabetes mellitus (T2DM) significantly increases the risk of cardiovascular disease and mortality. Mitochondrial dysfunction, in particular a reduction in mitochondrial DNA copy number (mtDNA-CN), plays an important role in the development of diabetic complications, including nephropathy. The aim of this study was to determine the mtDNA-CN in peripheral blood leukocytes of patients with T2DM depending on the presence of CKD. A total of 109 individuals were examined, including 20 healthy controls and 89 patients with T2DM divided into groups based on the presence or absence of CKD. The mtDNA-CN in leukocytes was determined using quantitative real-time PCR. Biochemical markers of T2DM and CKD were evaluated, non-parametric tests and correlation analysis were performed. No statistically significant differences in mtDNA-CN level were observed between patients with T2DM and CKD, patients with T2DM without CKD, and the control group (P > 0.05). No associations between mtDNA-CN and kidney function parameters were identified. The absence of mtDNA-CN alterations is assumed to contribute to the relatively satisfactory glycemic control in diabetic groups.