Nonlinear association between atherogenic index of plasma and chronic kidney disease: a nationwide cross-sectional study

Wang, Bo; Jiang, Chunqi; Qu, Yinuo; Wang, Jun; Yan, Chuanzhu; Zhang, Xin

doi:10.1186/s12944-024-02288-6

Lipids Health Dis

2024

DOI: 10.1186/s12944-024-02288-6

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Nonlinear association between atherogenic index of plasma and chronic kidney disease: a nationwide cross-sectional study

Bo Wang,

Chunqi Jiang,

Yinuo Qu

et al.

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2024

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Cited by 1 publication

References 28 publications

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Mitochondrial Dysfunction and Ion Imbalance in a Rat Model of Hemodialysis-Induced Myocardial Stunning

Nie,

Lin,

Yang

et al. 2024

Biomedicines

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Background/Objectives: Hemodialysis-induced myocardial stunning (HIMS) is a frequent complication in patients undergoing maintenance hemodialysis, characterized by transient left ventricular dysfunction due to ischemic episodes. Mitochondrial dysfunction and fluctuations in key ions such as potassium (K+) and calcium (Ca2+) are implicated in the pathogenesis of HIMS. This study aims to investigate the role of mitochondrial dysfunction and the protective potential of mitochondrial ATP-sensitive potassium channels (mitoKATP) in mitigating HIMS. Methods: A 5/6 nephrectomy rat model was established to mimic chronic kidney disease and the subsequent HIMS. The effects of mitoKATP channel modulators were evaluated by administering diazoxide (DZX), a mitoKATP opener, and 5-hydroxydecanoate (5-HD), a mitoKATP blocker, before hemodialysis. Mitochondrial function was assessed by measuring membrane potential, ATP synthase activity, and intramitochondrial Ca2+ levels. Myocardial function was evaluated using speckle tracking echocardiography. Results: Rats undergoing hemodialysis exhibited significant reductions in left ventricular strain and synchrony. DZX administration significantly improved mitochondrial function and reduced myocardial strain compared to controls. Conversely, 5-HD worsened mitochondrial swelling and disrupted myocardial function. Higher K+ and Ca2+ concentrations in the dialysate were associated with improved mitochondrial energy metabolism and myocardial strain. Conclusions: Mitochondrial dysfunction and ion imbalances during hemodialysis are key contributors to HIMS. The activation of mitoKATP channels provides mitochondrial protection and may serve as a potential therapeutic strategy to mitigate HIMS.

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Mitochondrial Dysfunction and Ion Imbalance in a Rat Model of Hemodialysis-Induced Myocardial Stunning

Nie,

Lin,

Yang

et al. 2024

Biomedicines

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show abstract

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Nonlinear association between atherogenic index of plasma and chronic kidney disease: a nationwide cross-sectional study

Cited by 1 publication

References 28 publications

Mitochondrial Dysfunction and Ion Imbalance in a Rat Model of Hemodialysis-Induced Myocardial Stunning

Mitochondrial Dysfunction and Ion Imbalance in a Rat Model of Hemodialysis-Induced Myocardial Stunning

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