scholarly journals Dietary Lipids and Dyslipidemia in Chronic Kidney Disease

Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 3138
Author(s):  
Zdzislaw Kochan ◽  
Natalia Szupryczynska ◽  
Sylwia Malgorzewicz ◽  
Joanna Karbowska

The progression of chronic kidney disease (CKD) leads to altered lipid metabolism. CKD patients exhibit high blood triglyceride (TG) levels, reduced concentrations and functionality of high-density lipoproteins (HDL), and elevated levels of atherogenic small, dense, low-density lipoproteins (sdLDL). Disorders of lipid metabolism and other metabolic disturbances place CKD patients at high risk for cardiovascular disease (CVD). Extensive evidence supports the cardioprotective effects of unsaturated fatty acids, including their beneficial effect on serum cholesterol and TG levels. Dietary lipids might therefore be especially important in the nutritional management of CKD. We review current dietary recommendations for fat intake by CKD patients and suggest potential nutritional interventions by emphasizing dietary lipids that might improve the blood lipid profile and reduce cardiovascular risk in CKD.

2020 ◽  
Author(s):  
Jian Liu ◽  
Geping Yu ◽  
Xialian Yu ◽  
Yunzi Liu ◽  
Weiming Wang

Abstract Background: Prevalence of dyslipidemia in china is rising and the pattern of dyslipidemia in china is different from western countries. Our study aimed to investigate the association between hyperlipidemia and chronic kidney disease in the general population.Methods: We conducted a retrospective, longitudinal cohort study of a health examination center database in China. Subjects who had at least three visits from 2011 to 2018 with normal baseline eGFR were enrolled. We evaluated the association of the lipid parameters with the incident chronic kidney diseases. Results: Totally, 8087 participants without kidney damage were identified. After the mean 5.51 years follow-up, 211 participants developed chronic kidney disease. Compared to non-CKD, participants developing CKD had lower baseline HDL-c (1.35±0.36 vs 1.24±0.36 mmol/L, p<0.001) and higher Lg(triglyceride) (0.15±0.27 vs 0.19±0.24, p=0.037). There was no difference of LDL-c (2.72±0.72 vs 2.72±0.71 mmol/L, p= 0.971) and total cholesterol (4.86±0.92 vs 4.80±0.89 mmol/L, p= 0.329) in two groups. Multi-variable logistic analysis showed that lower HDL-c was an independent risk of incident CKD (OR [95%] =1.61[1.02, 2.55], P=0.04) in participants.Conclusion: A lower HDL-c affects incident CKD in Chinese general population.


2020 ◽  
Vol 0 (1-2) ◽  
pp. 112-120
Author(s):  
В. Є. Кондратюк ◽  
А. С. Петрова ◽  
О. В. Карпенко ◽  
Т. Г. Осташевська ◽  
Е. К. Красюк

The results of a number of studies have proved the relationship between the functional state of the pineal gland and renal function. However, violations of the melatonin-forming function of the epiphysis (MFE) in patients with chronic kidney disease (CKD) undergoing hemodialysis (HD) and its relationship with dyslipidemia in this patient population is a poorly understood issue. The objective: to analyze disorders of MFE and blood lipid spectrum in patients with CKD of 5 stage treated with HD and to determine the relationship of epiphysis dysfunction with dyslipidemia. Materials and methods. 130 people (50% of men) aged 58.5 were surveyed [43; 66] which are on permanent hemodialysis treatment. Control passed 20 healthy individuals. The determination of day and night level of melatonin (MT) in saliva was conducted, based on the level of which patients (treated with HD) were divided into two groups: group I – 110 patients with impaired MFE, group II – 20 patients with normal MFE. Clinical and laboratory researches were carried out for all patients: general and biochemical analyzes of blood with determination of cholesterol level and its fractions, measurements of office blood pressure (BP) were made. Results. Significant prevalence of MFE disorders in patients with CKD of 5 stage treated with hemodialysis and its relationship with blood lipid spectrum were found. The level of total cholesterol (TC), triglycerides (TG) and low density lipoproteins (LDL) in patients with impaired MFE was higher by 26.4 % (p<0.05), 16.7 % (p<0.05) and 22,6 % (p= 0.03) according to the outcome of the comparison group patients. The level of high-density lipoprotein (HDL) of the main group is lower by 11.8 % compared to the group with preserved MFE. The data obtained indicate the relationship of MFE disorders with the duration of RRT treatment, the duration of arterial hypertension, the age of patients, and their effect on the lipid spectrum of patients with CKD of 5 stage treated with hemodialysis. Night feedback correlation of MT with TC level was established (r=–0.256; p<0.05). Correlation analysis confirms that a decrease in MT at night is combined with an increase of TG level (r=–0.272; p<0.05) in the blood of patients. The feedback correlation of night (r=–0.347; p=0.03) and daytime level (r=–0.198; p<0.05) of MT with LDL level and positive relationships between MT in daytime (r=0.27; p=0.03) and the night period (r=0.331; p=0.02) with HDL levels. Conclusion. For patients with CKD of 5 stage undergoing hemodialysis, there is a frequent violation of MFE (84.6%) and significant disorders of lipid metabolism (58%). Analysis of the lipid metabolism study revealed more profound abnormalities in the form of an increased concentration of TC and all its fractions in patients with impaired MFE, which may indicate a connection between epiphysis dysfunction and lipid metabolism in patients with RRT. In patients with hemodialysis, melatonin-forming dysfunction and disorders of lipid metabolism are age-dependent and are determined by the duration of RRT, the duration of hypertension, the level of hemoglobin. We have identified a relationship between the deterioration of lipid metabolism on the background of deeper disturbance of MFE by daytime and nighttime MT.


Author(s):  
M. I. Chaikovska ◽  
L. P. Martynyuk

Recent scientificstudies have demonstrated the effect of fibroblast growth factor 23 (FGF-23) on the volume and distribution of body fat. The aim of our study was to investigate of lipid metabolism in patients with chronic kidney disease (CKD) and its relationship with FGF-23. Methods. We conducted a single-center, cohort retrospective study involved 106 patients with CKD 1-5 stages. Among the patients were 47 women (44%) and 59 men (56%) aged (49.6±13.9) years. All patients were determined the blood lipid spectrum: total cholesterol level (LDL), high density lipoproteins (HDL) and triglycerides (TG). The lipid profile was examined using a biochemical analyzer Cobas Integra 400 Plus. The C-terminal FGF-23 fragment was determined using a set of reagents for the enzyme immunoassay “Biomedica” (Astria). The glomerular filtration rate (GFR) was calculated using the CKD EPI formula (KDIGO 2012). All the statistical analyses were performed using Statistica 10.0. Results. In patients with CKD, progressive decrease in the level of total cholesterol, LDL cholesterol, HDL cholesterol and the increase in TG concurrent with the fall in GFR was detected (p<0.001). The concentration of the C-terminal FGF-23 fragment progressively increased in parallel with the fall in GFR, reaching the highest values at CKD stage 5 (p<0.001). A significant relationship was found between FGF-23 and total cholesterol (r =-0.45, p<0.05), LDL (r=-0.29, p<0.05), HDL (r=-0.54, p<0.05), FGF-23 and TG (r=0.28, p<0.05). Conclusions. CKD is characterized by a significant growth in TG levels, which increases with progression of renal dysfunction. The level of FGF-23 in CKD steadily increases in parallel with the decrease in GFR. The parameters of lipid metabolism, namely, total cholesterol, LDL, TG and HDL, have a reliable relationship with FGF-23 in CKD.


Author(s):  
Ayasa Ochiai ◽  
Mahmoud Ben Othman ◽  
Kazuichi Sakamoto

Abstract Kaempferol (KPF) is a dietary polyphenol reported to have various beneficial effects on human health. However, its molecular mechanisms in regulating lipid and glucose metabolism are not fully understood. This study examined the effects of KPF on obesity, dyslipidemia, and diabetes in Tsumura, Suzuki, Obese Diabetes (TSOD) mice. The six-week administration of KPF decreased fat weight, serum total cholesterol, and low-density lipoproteins (LDLs); increased high-density lipoproteins (HDLs); and improved glucose tolerance. Additionally, KPF increased LDL receptor (LDLR) and apolipoprotein A1 (ApoA1) gene expression and decreased serum resistin levels. These findings suggest that the decrease in LDL and the increase in HDL caused by KPF may be due to increases in hepatic LDLR and ApoA1 expression, respectively. Furthermore, it is possible that the improvement in glucose tolerance by KPF may occur via resistin reduction. These mechanisms may be parts of complex mechanism by which KPF improves metabolic syndrome.


2020 ◽  
Author(s):  
Xudong Liang ◽  
Meiyu Ye ◽  
Mei Tao ◽  
Danna Zheng ◽  
Ruyi Cai ◽  
...  

Abstract Background According to the "lipid nephrotoxicity hypothesis", there is now significant research being conducted in this area. By studying the role of hyperlipidemia in chronic kidney disease in the general Zhejiang population, we aimed to explore the correlation between changes in blood lipid levels and chronic kidney disease.Methods We collected and analyzed clinical data from ordinary residents who participated in the annual comprehensive physical examination with no overt kidney disease in Zhejiang Provincial People's Hospital, China from January 2011 to December 2016. According to triglyceride, total cholesterol and low-density lipoprotein levels, participants were respectively divided into 4 groups. Statistical methods were used to evaluate the correlation between different blood lipid profiles and chronic kidney disease.Results 5,183 participants were included in our study. During the six-year follow-up period, 227 participants (4.4%) developed chronic kidney disease. The odds ratio for incident chronic kidney disease was 3.14 (95%CI: 1.53–6.43) in Q3, 3.84 (95%CI: 1.90–7.76) in Q4 according to the total cholesterol group and 1.17 (95%CI: 1.04–1.32) in Q3, 1.40 (95%CI: 1.11–2.48) in Q4 according to the low-density lipoprotein group, respectively, after multivariable-adjusted analyses. According to the triglyceride grouping, the odds ratio for incident chronic kidney disease was 2.88 (95%CI: 1.29-6.43) in Q2, 2.92 (95%CI: 1.44–6.57) in Q3 and 3.08 (95%CI: 1.11–6.69) in Q4, after multivariable-adjusted analyses.Conclusion Increased triglycerides and high levels of total cholesterol and low-density lipoprotein were independently associated with an increased likelihood of eGFR decline and development of incident chronic kidney disease in the general Zhejiang population.


Toxins ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 671 ◽  
Author(s):  
Florens ◽  
Calzada ◽  
Delolme ◽  
Page ◽  
Guebre Egziabher ◽  
...  

Chronic kidney disease is associated with an increased cardiovascular risk, and altered biological properties of high-density lipoproteins (HDL) may play a role in these events. This study aimed to describe the HDL proteome from non-diabetic hemodialysis patients and identify potential pathways affected by the dysregulated expression of HDL proteins. HDL were sampled from nine non-diabetic hemodialysis (HD) and eight control patients. Samples were analyzed using a nano-RSLC coupled with a Q-Orbitrap. Data were processed by database searching using SequestHT against a human Swissprot database and quantified with a label-free quantification approach. Proteins that were in at least five of the eight control and six of the nine HD patients were analyzed. Analysis was based on pairwise ratios and the ANOVA hypothesis test. Among 522 potential proteins, 326 proteins were identified to be in the HDL proteome from HD and control patients, among which 10 were significantly upregulated and nine downregulated in HD patients compared to the control patients (p < 0.05). Up and downregulated proteins were involved in lipid metabolism, hemostasis, wound healing, oxidative stress, and apoptosis pathways. This difference in composition could partly explain HDL dysfunction in the chronic kidney disease (CKD) population and participate in the higher cardiovascular risk observed in this population.


2018 ◽  
Vol 237 (2) ◽  
pp. 175-191 ◽  
Author(s):  
Jung-Yoon Heo ◽  
Ji-Eun Kim ◽  
Yongwook Dan ◽  
Yong-Woon Kim ◽  
Jong-Yeon Kim ◽  
...  

Clusterin is a secretory glycoprotein that is involved in multiple physiopathological processes, including lipid metabolism. Previous studies have shown that clusterin prevents hepatic lipid accumulation via suppression of sterol regulatory element-binding protein (SREBP) 1. In this study, we examined the role of clusterin in renal lipid accumulation in clusterin-knockout mice and NRK52e tubular epithelial cells. Clusterin deficiency increased the expression of SREBP1 and its target genes and decreased malonyl-CoA decarboxylase protein levels in the kidney. Expression of the endocytic receptor, megalin, and scavenger receptor class A was increased in clusterin-deficient mice. Functional analysis of lipid metabolism also revealed that lipid uptake and triglyceride synthesis were increased and fatty acid oxidation was reduced, leading to increased lipid accumulation in clusterin-deficient mice. These phenomena were accompanied by mesangial expansion, fibrosis and increased urinary protein-to-creatinine ratio. High-fat feeding aggravated these clusterin deficiency-induced pathological changes. Clusterin knockdown in NRK52e cells increased lipogenic gene expression and lipid levels, whereas overexpression of clusterin by treatment with adenovirus or recombinant clusterin protein suppressed lipogenic gene expression and lipid levels. Transforming growth factor-beta 1 (TGFB1) expression increased in the kidney of clusterin-deficient mice and suppression of TGFB1 in NRK52e cells suppressed lipid accumulation. These results suggest that clusterin deficiency induces renal lipid accumulation by dysregulating the expression of lipid metabolism-related factors and TGFB1, thereby leading to chronic kidney disease. Hence, clusterin may serve as a therapeutic target for lipid-induced chronic kidney disease.


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