| 초록 |
Objectives: Mitokines are released in response to cellular stress and play important roles in metabolic and physiological processes. Finerenone, a non-steroidal mineralocorticoid receptor antagonist, is a cornerstone therapy for diabetic kidney disease (DKD). This study aimed to investigate the effects of finerenone on circulating mitokine levels in individuals with DKD. Methods: Individuals with finerenone-naïve DKD (n = 42; 88.1% receiving sodium–glucose cotransporter 2 inhibitors) and healthy controls (n = 35) were prospectively enrolled. Circulating levels of fibroblast growth factor 21 (FGF21), growth differentiation factor 15 (GDF15), humanin, and mitochondrial open reading frame of the 12S rRNA-c (MOTS-c) were measured using ELISA. In individuals with DKD, mitokine levels were reassessed at 3 and 6 months after initiation of finerenone treatment. Results: Individuals with DKD were older and had a higher body mass index and albuminuria, and a lower estimated glomerular filtration rate (all P < 0.001). Compared with healthy controls, GDF15 levels were lower, whereas FGF21 and humanin levels were higher, in the finerenone group (all P < 0.001; Fig. 1). MOTS-c levels did not differ between the groups (P = 0.250; Fig. 1). After finerenone treatment, humanin levels decreased at 3 months but increased again at 6 months (all P < 0.001). In addition, at 6 months, GDF15 and MOTS-c levels increased, while FGF21 levels decreased (all P < 0.001). At 6 months of finerenone treatment, 71.43% of patients achieved a ≥30% reduction in albuminuria, and there were no differences in circulating mitokine levels between patients with and without a ≥30% reduction in albuminuria. Conclusion: DKD is associated with dysregulated circulating mitokine levels. Finerenone treatment resulted in dynamic changes in mitokine levels, which appeared after 3 months of treatment. These findings suggest that finerenone therapy may mitigate mitochondrial dysfunction in individuals with DKD. |