Serum coenzyme <scp>Q</scp>10 levels are associated with coronary flow reserve in hemodialysis patients

Macunluoğlu, Beyza; Kaya, Yüksel; Atakan, Aydın; Arı, Elif; Kaspar, Çiğdem; Demır, Halit; Hakan, Hamit; Aşıcıoğlu, Ebru; Kedrah, Alla Eldeen

doi:10.1111/hdi.12001

Cited by 10 publications

(7 citation statements)

References 30 publications

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“…25–28 Second, patients undergoing MHD are known to have low plasma CoQ 10 levels compared to age- and sex-matched healthy individuals, and that these levels are associated with reduced coronary blood flow. 17,29 Third, previous data from a non-randomized CoQ 10 dose escalation study in MHD patients confirmed that doses as high as 1800mg per day were safe and well-tolerated, and suggested that CoQ 10 supplementation may be associated with improvements in oxidative stress burden in these individuals. 30 Finally, prior studies have shown that in patients with kidney disease, perturbations in cell metabolism lead to preferential dysregulation of mitochondrial respiratory machinery that is closely associated with the enhanced oxidative stress seen in these individuals.…”

Section: Discussionmentioning

confidence: 91%

Effect of Coenzyme Q10 on Biomarkers of Oxidative Stress and Cardiac Function in Hemodialysis Patients: The CoQ10 Biomarker Trial

Rivara

Yeung

Robinson‐Cohen

et al. 2017

American Journal of Kidney Diseases

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Background Oxidative stress is highly prevalent in patients with end-stage renal disease and is linked to excess cardiovascular risk. Identifying therapies that reduce oxidative stress has the potential to improve cardiovascular outcomes in patients undergoing maintenance dialysis. Study Design Placebo-controlled, three-arm, double-blind, randomized, clinical trial Setting & Participants 65 patients undergoing thrice-weekly maintenance hemodialysis Intervention Patients were randomly assigned in a 1:1:1 ratio to receive once daily CoQ10 (600 mg or 1200 mg) or matching placebo for 4 months. Outcomes The primary outcome was plasma oxidative stress, defined as plasma concentration of F2-isoprotanes. Secondary outcomes included plasma isofurans, cardiac biomarkers, pre-dialysis blood pressure, and safety/tolerability. Measurements F2-isoprostanes and isofurans were measured as plasma markers of oxidative stress, and N-terminal-pro-b-type natriuretic peptide and troponin T were measured as cardiac biomarkers at baseline, 1, 2, and 4 months. Results Among 80 patients randomized, 15 were excluded due to not completing at least one post-baseline study visit, and 65 were included in the primary intention-to-treat analysis. No treatment-related major adverse events occurred. Daily treatment with 1200 mg but not 600 mg CoQ10 significantly reduced plasma concentrations of F2-isoprostanes at 4 months compared to placebo (adjusted mean change −10.7 pg/ml [95% CI −7.1 to −14.3 pg/mL], P < 0.001; and −8.3 pg/ml [95% CI −5.5 to −11.0 pg/ml], P = 0.1, respectively). There were no significant effects of CoQ10 treatment on plasma isofurans, cardiac biomarker concentrations, or pre-dialysis blood pressures. Limitations Study not powered to detect small treatment effects; difference in baseline characteristics among randomized groups. Conclusions In patients undergoing maintenance hemodialysis, daily supplementation with 1200 mg of CoQ10 is safe and results in a reduction in plasma concentrations of F2-isoprostanes, a marker of oxidative stress. Future studies are needed to determine whether CoQ10 supplementation improves clinical outcomes for patients undergoing maintenance hemodialysis.

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Section: Discussionmentioning

confidence: 91%

Effect of Coenzyme Q10 on Biomarkers of Oxidative Stress and Cardiac Function in Hemodialysis Patients: The CoQ10 Biomarker Trial

Rivara

Yeung

Robinson‐Cohen

et al. 2017

American Journal of Kidney Diseases

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“…Additionally, epicardial fat tissue (EFT), the visceral adipose tissue surrounding the subepicardial coronary vessels has recently been recognized as a new risk factor for atherosclerotic heart disease in PD and HD patients [ 93 , 94 ]. EFT is a lipid-storing depot [ 95 , 96 ] and secretes proatherosclerotic and proinflammatory cytokines [ 97 – 99 ].…”

Section: Endogenous and Food Derived Antioxidantsmentioning

confidence: 99%

Mitochondria: a new therapeutic target in chronic kidney disease

et al. 2015

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Cellular metabolic changes during chronic kidney disease (CKD) may induce higher production of oxygen radicals that play a significant role in the progression of renal damage and in the onset of important comorbidities. This condition seems to be in part related to dysfunctional mitochondria that cause an increased electron “leakage” from the respiratory chain during oxidative phosphorylation with a consequent generation of reactive oxygen species (ROS).ROS are highly active molecules that may oxidize proteins, lipids and nucleic acids with a consequent damage of cells and tissues.To mitigate this mitochondria-related functional impairment, a variety of agents (including endogenous and food derived antioxidants, natural plants extracts, mitochondria-targeted molecules) combined with conventional therapies could be employed.However, although the anti-oxidant properties of these substances are well known, their use in clinical practice has been only partially investigated. Additionally, for their correct utilization is extremely important to understand their effects, to identify the correct target of intervention and to minimize adverse effects.Therefore, in this manuscript, we reviewed the characteristics of the available mitochondria-targeted anti-oxidant compounds that could be employed routinely in our nephrology, internal medicine and renal transplant centers. Nevertheless, large clinical trials are needed to provide more definitive information about their use and to assess their overall efficacy or toxicity.

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“…Similarly, plasma CoQ10 levels have been reported to be significantly lower in chronic kidney disease (CKD) patients (with or without haemodialysis), compared to healthy controls [ 80 , 81 , 82 ]. CoQ10 supplementation may improve renal function and reduce the need for dialysis in patients with CKD.…”

Section: Supplementation With Coq10mentioning

confidence: 99%

Disorders of Human Coenzyme Q10 Metabolism: An Overview

Hargreaves

Heaton

Mantle

2020

IJMS

107

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Coenzyme Q10 (CoQ10) has a number of vital functions in all cells, both mitochondrial and extramitochondrial. In addition to its key role in mitochondrial oxidative phosphorylation, CoQ10 serves as a lipid soluble antioxidant, plays an important role in fatty acid, pyrimidine and lysosomal metabolism, as well as directly mediating the expression of a number of genes, including those involved in inflammation. In view of the central role of CoQ10 in cellular metabolism, it is unsurprising that a CoQ10 deficiency is linked to the pathogenesis of a range of disorders. CoQ10 deficiency is broadly classified into primary or secondary deficiencies. Primary deficiencies result from genetic defects in the multi-step biochemical pathway of CoQ10 synthesis, whereas secondary deficiencies can occur as result of other diseases or certain pharmacotherapies. In this article we have reviewed the clinical consequences of primary and secondary CoQ10 deficiencies, as well as providing some examples of the successful use of CoQ10 supplementation in the treatment of disease.

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Serum coenzyme Q10 levels are associated with coronary flow reserve in hemodialysis patients

Cited by 10 publications

References 30 publications

Effect of Coenzyme Q10 on Biomarkers of Oxidative Stress and Cardiac Function in Hemodialysis Patients: The CoQ10 Biomarker Trial

Effect of Coenzyme Q10 on Biomarkers of Oxidative Stress and Cardiac Function in Hemodialysis Patients: The CoQ10 Biomarker Trial

Mitochondria: a new therapeutic target in chronic kidney disease

Disorders of Human Coenzyme Q10 Metabolism: An Overview

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