Abstract
BackgroundChronic kidney disease (CKD) is a major challenge for public health due to increased risk of cardiovascular diseases (CVD) and premature death. The aim of this study was to determine the clinical picture of FA and the course of the pathophysiological mechanisms of CKD.MethodsThe study involved 149 patients with CKD and a control group including 43 people. Fatty acid profiles were investigated using gas chromatography. A total of 30 fatty acids and their derivatives were identified and quantified. The omega3, omega6, SFA, MUFA, and PUFA fatty acid contents were calculated. The correlation matrix was obtained for parameters relating to patients with CKD vs. FA, taking patients’ sex into consideration. The index C18:3n6/C22:4n6 was calculated according to the length of the treatment. Statistica 12.0 software (Tulsa, Oklahoma, USA) was used for the statistical analyses.ResultsThe results showed decreased levels of total PUFA and increased concentrations of MUFA, including the activation of the palmitic and oleic acid pathway. An increase in the levels of n-6 9C22: 4n6 family fatty acids in all the patients and a reduction in the n-3 family (EPA, DHA) were observed. C18:3n6 was negatively correlated and C22:4n6 was positively correlated with the duration of the treatment. The index C18:3n6/C22:4n6 was defined as a new marker in the progression of the disease. Moreover, the index C18:3n6/ C22:4n6 was drastically decreased in later period. Nervonic acid was higher in the CKD group. In the group of men with CKD, there was a negative correlation between the excretion of K+, anthropometric measurements, and the levels of EPA and DHA.ConclusionsThe course of inflammation in CKD occurs through the decrease in PUFA and the synthesis of MUFA. The dominating cascade of changes is the elongation of GLA-C18:3n6 into DGLA-C20:3n6 and AA-C20:4n6. As CKD progresses, along with worsening anthropometrical parameters and increased secretion of potassium, the activity of Ʌ6-desaturase decreases, reducing the synthesis of EPA and DHA. The synthesis of AdA-C22:4n6 increases and the ratio C18:3n6/C22:4n6 drastically decreases after 5 years. This parameter can be used to diagnose disease progression.
Highlights
Chronic kidney disease (CKD) is a major challenge for public health due to increased risk of cardiovascular diseases (CVD) and premature death
Highlights We present a clinical picture of free fatty acid (FFA) and the course of the pathophysiological mechanisms of chronic kidney disease (CKD)
The authors of the study already compared the fatty acids (FA) profile of CKD patients with the profile of patients with Metabolic Syndrome (MetS); it was observed that there had been an increase in the amounts of all FAs in plasma in the CKD group, especially in the case of palmitic acid (C16:0) and the derivatives of stearic acid (C18:0), higher than in the MetS patients; this may result from the decomposition of adipose tissue and the progressing devastation of the organism [11]
Summary
Chronic kidney disease (CKD) is a major challenge for public health due to increased risk of cardiovascular diseases (CVD) and premature death. Our studies show that in patients with CKD the concentration of FA in plasma is dependent on the stage of the disease and the catabolism of adipose tissue, which takes part in the progression of inflammation and is the cause of CKD development Such a conclusion was drawn by other researchers: Afshinnia et al connected an increased level of saturated FA C16:0-C20:0 with impaired β-oxidation of FA and reverse partitioning/binding into complex lipids as mechanisms facilitating changes in lipid metabolism which characterize progressing CKD [5]. Non-alcoholic fatty liver disease (NAFLD) may be a risk factor for diabetic nephropathy (DN), and increased fat content in liver may be connected to higher DN risk [7] These results are not consistent among various researchers. The higher increase of nervonic acid (C24:1) in CKD suggests a higher degree of demyelination and loss of anons [11]
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