Platelet Mitochondrial Respiration, Endogenous Coenzyme Q(10) and Oxidative Stress in Patients with Chronic Kidney Disease

慢性肾脏病患者的血小板线粒体呼吸、内源性辅酶Q10和氧化应激

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Abstract

Chronic kidney disease (CKD) is characterized by a progressive loss of renal function and a decrease of glomerular filtration rate. Reduced mitochondrial function, coenzyme Q(10) (CoQ(10)), and increased oxidative stress in patients with CKD contribute to the disease progression. We tested whether CoQ(10) levels, oxidative stress and platelet mitochondrial bioenergetic function differ between groups of CKD patients. METHODS: Twenty-seven CKD patients were enrolled in this trial, 17 patients had arterial hypertension (AH) and 10 patients had arterial hypertension and diabetes mellitus (AH and DM). The control group consisted of 12 volunteers. A high-resolution respirometry (HRR) method was used for the analysis of mitochondrial bioenergetics in platelets, and an HPLC method with UV detection was used for CoQ(10) determination in platelets, blood, and plasma. Oxidative stress was determined as thiobarbituric acid reactive substances (TBARS). RESULTS: Platelets mitochondrial respiration showed slight, not significant differences between the groups of CKD patients and control subjects. The oxygen consumption by intact platelets positively correlated with the concentration of CoQ(10) in the platelets of CKD patients. CONCLUSION: A decreased concentration of CoQ(10) and oxidative stress could contribute to the progression of renal dysfunction in CKD patients. The parameters of platelet respiration assessed by high-resolution respirometry can be used only as a weak biological marker for mitochondrial diagnosis and therapy monitoring in CKD patients.

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