Showing papers on "High-density lipoprotein published in 2015"
TL;DR: Evidence is provided that vegetarian diets effectively lower blood concentrations of total cholesterol, low‐density lipoprotein cholesterol, high‐ density lipop Protein cholesterol, and non–high‐density cholesterol cholesterol, which could be a useful nonpharmaceutical means of managing dyslipidemia, especially hypercholesterolemia.
Abstract: Background Vegetarian diets exclude all animal flesh and are being widely adopted by an increasing number of people; however, effects on blood lipid concentrations remain unclear. This meta‐analysis aimed to quantitatively assess the overall effects of vegetarian diets on blood lipids.
Methods and Results We searched PubMed, Scopus, Embase, ISI Web of Knowledge, and the Cochrane Library through March 2015. Studies were included if they described the effectiveness of vegetarian diets on blood lipids (total cholesterol, low‐density lipoprotein cholesterol, high‐density lipoprotein cholesterol, and triglyceride). Weighted mean effect sizes were calculated for net changes by using a random‐effects model. We performed subgroup and univariate meta‐regression analyses to explore sources of heterogeneity. Eleven trials were included in the meta‐analysis. Vegetarian diets significantly lowered blood concentrations of total cholesterol, low‐density lipoprotein cholesterol, high‐density lipoprotein cholesterol, and non–high‐density lipoprotein cholesterol, and the pooled estimated changes were −0.36 mmol/L (95% CI −0.55 to −0.17; P <0.001), −0.34 mmol/L (95% CI −0.57 to −0.11; P <0.001), −0.10 mmol/L (95% CI −0.14 to −0.06; P <0.001), and −0.30 mmol/L (95% CI −0.50 to −0.10; P =0.04), respectively. Vegetarian diets did not significantly affect blood triglyceride concentrations, with a pooled estimated mean difference of 0.04 mmol/L (95% CI −0.05 to 0.13; P =0.40).
Conclusions This systematic review and meta‐analysis provides evidence that vegetarian diets effectively lower blood concentrations of total cholesterol, low‐density lipoprotein cholesterol, high‐density lipoprotein cholesterol, and non–high‐density lipoprotein cholesterol. Such diets could be a useful nonpharmaceutical means of managing dyslipidemia, especially hypercholesterolemia.
222 citations
TL;DR: Ex vivo studies showed that patients with NAFLD had increased sensitivity of hepatic triglyceride levels and cholesterol synthesis to insulin, and that sensitivity increased the development of cirrhosis.
166 citations
TL;DR: Clearance of HCV using an IFN‐free antiviral regimen results in rapid changes in peripheral and intrahepatic metabolic pathways, implicating a direct effect ofHCV replication on lipid homeostasis.
132 citations
TL;DR: Male gender is associated with a more atherogenic profile than female gender, with appreciably lower levels of the HDL2-C subfraction, among women, but has less effect than male gender.
126 citations
TL;DR: The evidence for HDL anti-oxidative function and the potential contributions of apolipoproteins, lipid transfer proteins, paraoxonases and other enzymes associated with HDL are reviewed.
Abstract: High-density lipoprotein (HDL) provides a pathway for the passage of lipid peroxides and lysophospholipids to the liver via hepatic scavenger receptors. Perhaps more importantly, HDL actually metabolizes lipid hydroperoxides preventing their accumulation on low-density lipoprotein (LDL), thus impeding its atherogenic structural modification. A number of candidates have been suggested to be responsible for HDL's antioxidant function, with paraoxonase-1 (PON1) perhaps the most prominent. Here we review the evidence for HDL anti-oxidative function and the potential contributions of apolipoproteins, lipid transfer proteins, paraoxonases and other enzymes associated with HDL.
100 citations
TL;DR: In the present analysis, a higher TG/HDL-C ratio was associated with an increasingly atherogenic lipid phenotype, characterized by higher RLP-C along with higher non-HDl-C and LDL density.
96 citations
TL;DR: More kinetic studies are required to obtain a more complete understanding of the fasting and postprandial lipoprotein metabolism caused by phytosterols and phytostanols.
Abstract: The efficacy of phytosterols and phytostanols added to foods and food supplements to obtain significant non-pharmacologic serum and low density lipoprotein (LDL) cholesterol reduction is well documented. Irrespective of age, gender, ethnic background, body weight, background diet, or the cause of hypercholesterolemia and, even added to statin treatment, phytosterols and phytostanols at 2 g/day significantly lower LDL cholesterol concentration by 8%–10%. They do not affect the concentrations of high density lipoprotein cholesterol, lipoprotein (a) or serum proprotein convertase subtilisin/kexin type 9. In some studies, phytosterols and phytostanols have modestly reduced serum triglyceride levels especially in subjects with slightly increased baseline concentrations. Phytosterols and phytostanols lower LDL cholesterol by displacing cholesterol from mixed micelles in the small intestine so that cholesterol absorption is partially inhibited. Cholesterol absorption and synthesis have been carefully evaluated during phytosterol and phytostanol supplementation. However, only a few lipoprotein kinetic studies have been performed, and they revealed that LDL apoprotein B-100 transport rate was reduced. LDL particle size was unchanged, but small dense LDL cholesterol concentration was reduced. In subjects with metabolic syndrome and moderate hypertriglyceridemia, phytostanols reduced not only non- high density lipoprotein (HDL) cholesterol concentration but also serum triglycerides by 27%, and reduced the large and medium size very low density lipoprotein particle concentrations. In the few postprandial studies, the postprandial lipoproteins were reduced, but detailed studies with apoprotein B-48 are lacking. In conclusion, more kinetic studies are required to obtain a more complete understanding of the fasting and postprandial lipoprotein metabolism caused by phytosterols and phytostanols. It seems obvious, however, that the most atherogenic lipoprotein particles will be diminished.
90 citations
TL;DR: In people with very high HDL-C, reduced HDL phospholipid content and cholesterol efflux capacity are associated with the paradoxical development of CAD.
Abstract: Objective— Plasma levels of high-density lipoprotein cholesterol (HDL-C) are strongly inversely associated with coronary artery disease (CAD), and high HDL-C is generally associated with reduced risk of CAD. Extremely high HDL-C with CAD is an unusual phenotype, and we hypothesized that the HDL in such individuals may have an altered composition and reduced function when compared with controls with similarly high HDL-C and no CAD.
Approach and Results— Fifty-five subjects with very high HDL-C (mean, 86 mg/dL) and onset of CAD at the age of ≈60 years with no known risk factors for CAD (cases) were identified through systematic recruitment. A total of 120 control subjects without CAD, matched for race, sex, and HDL-C level (controls), were identified. In all subjects, HDL composition was analyzed and HDL cholesterol efflux capacity was assessed. HDL phospholipid composition was significantly lower in cases (92±37 mg/dL) than in controls (109±43 mg/dL; P =0.0095). HDL cholesterol efflux capacity was significantly lower in cases (1.96±0.39) than in controls (2.11±0.43; P =0.04).
Conclusions— In people with very high HDL-C, reduced HDL phospholipid content and cholesterol efflux capacity are associated with the paradoxical development of CAD.
# Significance {#article-title-29}
90 citations
TL;DR: Evidence is provided that the β3-AR Trp64Arg and UCP1 -3826 A > G polymorphisms are associated with TG levels in overweight/obese Chinese subjects and that the two polymorphisms is also associated with certain lipid and apolipoprotein variations, depending on BMI.
Abstract: The beta-3 adrenergic receptor (β3-AR) Trp64Arg and uncoupling protein 1 (UCP1) -3826 A > G polymorphisms have been reported to be associated with obesity and/or lipid metabolism in some populations. This study examined the possible association of the β3-AR and UCP1 polymorphisms with overweight/obesity or lipid variation in a Southwest Chinese population. A total of 418 Han Chinese (249 overweight/obese and 169 healthy control subjects) in the Chengdu area were studied using PCR-RFLP analysis. Total serum cholesterol (TC) and triglycerides (TGs) were measured using an enzymatic method. High density lipoprotein cholesterol (HDL-C) was determined after sodium phosphotungstate/magnesium chloride precipitation of low-density lipoproteins by polyvinyl sulfate. Serum apolipoproteins were quantified by radial immunodiffusion. The genotype and allele frequencies of the β3-AR Trp64Arg and UCP1 -3826 A > G polymorphisms in overweight/obese subjects exhibited no significant differences compared to the controls. However, subjects carrying the β3-AR TrpTrp genotype and UCP1 AG genotype had higher TG levels than those carrying the Arg allele and AA genotype, respectively (P G polymorphisms are associated with TG levels in overweight/obese Chinese subjects and that the two polymorphisms are also associated with certain lipid and apolipoprotein variations, depending on BMI. However, these polymorphisms are not associated with overweight/obesity or low HDL-cholesterolemia in a Chinese population from the Chengdu area.
87 citations
TL;DR: This review examines disrupted cholesterol transport in CKD, presenting both clinical and preclinical evidence of the effect of the uremic environment on vascular lipid accumulation.
85 citations
TL;DR: It is concluded that thymol may exhibit promising anti-diabetic activity and protects C57BL/6J mice against HFD due to its anti- hyperglycaemic and anti-hyperlipidemic activity.
TL;DR: A mathematical model of plaque growth is developed which includes the (LDL, HDL) concentrations and is refined by including the effect of reverse cholesterol transport, which suggests that such drugs as used for mice may also slow plaque growth in humans.
TL;DR: Findings suggest LPPs are key factors underlying cardio-metabolic derangements that occur with obesity and that GPx4 serves a critical role as an adaptive countermeasure.
Abstract: Objective: Lipid peroxides and their reactive aldehyde derivatives (LPPs) have been linked to obesity-related pathologies, but whether they have a causal role has remained unclear. Glutathione peroxidase 4 (GPx4) is a selenoenzyme that selectively neutralizes lipid hydroperoxides, and human gpx4 gene variants have been associated with obesity and cardiovascular disease in epidemiological studies. This study tested the hypothesis that LPPs underlie cardio-metabolic derangements in obesity using a high fat, high sucrose (HFHS) diet in gpx4 haploinsufficient mice (GPx4 þ/� ) and in samples of human myocardium. Methods: Wild-type (WT) and GPx4 þ/� mice were fed either a standard chow (CNTL) or HFHS diet for 24 weeks, with metabolic and cardiovascular parameters measured throughout. Biochemical and immuno-histological analysis was performed in heart and liver at termination of study, and mitochondrial function was analyzed in heart. Biochemical analysis was also performed on samples of human atrial myocardium from a cohort of 103 patients undergoing elective heart surgery. Results: Following HFHS diet, WT mice displayed moderate increases in 4-hydroxynonenal (HNE)-adducts and carbonyl stress, and a 1.5-fold increase in GPx4 enzyme in both liver and heart, while gpx4 haploinsufficient (GPx4 þ/� ) mice had marked carbonyl stress in these organs accompanied by exacerbated glucose intolerance, dyslipidemia, and liver steatosis. Although normotensive, cardiac hypertrophy was evident with obesity, and cardiac fibrosis more pronounced in obese GPx4 þ/� mice. Mitochondrial dysfunction manifesting as decreased fat oxidation capacity and increased reactive oxygen species was also present in obese GPx4 þ/� but not WT hearts, along with up-regulation of pro-inflammatory and pro-fibrotic genes. Patients with diabetes and hyperglycemia exhibited significantly less GPx4 enzyme and greater HNE-adducts in their hearts, compared with age-matched non-diabetic patients. Conclusion: These findings suggest LPPs are key factors underlying cardio-metabolic derangements that occur with obesity and that GPx4 serves a critical role as an adaptive countermeasure.
Journal Article•
TL;DR: In this paper, the longitudinal association between changes in inflammation with advanced lipoprotein measurements and HDL cholesterol efflux capacity was determined. But, the authors did not find significant correlations between a reduction in hsCRP with increases in LDL (r=0.25,p=0,0.03), apoA1 (r = 0.27, p=0.,0.02, Figure 1a), HDL (r>0.24, p>0,02), an overall improvement of efflux Capacity of 5.7% (p=5
Abstract: Background: Potent anti-inflammatory RA treatments are associated with reduced cardiovascular (CV) risk as well as increases in low density lipoprotein (LDL). This apparent paradox may be explained by favorable changes in other lipid measurements. The objective of this study was to determine the longitudinal association between changes in inflammation with advanced lipoprotein measurements and HDL cholesterol efflux capacity.
Methods and Results: We conducted this study in a longitudinal RA cohort from a large academic center. We included subjects with hsCRP reduction ≥10mg/L at two time points one year apart. Subjects on statins during the study period or 6 months prior were excluded. We measured total cholesterol (TC), LDL, high density lipoprotein (HDL), apolipoprotein B (apoB), apoA1, and HDL cholesterol efflux capacity at baseline and one year follow-up. We determined the correlations between reduction in hsCRP and change in lipid parameters using the Pearson test.
We studied 90 RA subjects, mean age 57 years, 89% female, all subjects were on disease modifying anti-rheumatic drugs; median baseline hsCRP was 28.6mg/L and follow-up 4.3 mg/L (reduction of 85%, p<0.0001). We observed significant correlations between a reduction in hsCRP with increases in LDL (r=0.25,p=0.02, Figure 1a), HDL (r=0.23, p=0.03), apoA1 (r=0.27, p=0.01 and HDL cholesterol efflux capacity (r=0.24, p=0.02), an overall improvement of efflux capacity of 5.7% (p=5x10-4, Figure 1b).
Conclusion: Reduction in inflammation was associated increased LDL levels, and concomitant increases in HDL, ApoA1, and improvements in HDL cholesterol efflux capacity. These findings provide further insight into lipid modulation and the beneficial effect of reduction in inflammation on lipids in vivo.
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TL;DR: It is suggested that cholesterol efflux capacity (CEC) of human plasma or serum is a potent marker of ASCVD risk and that CEC may be a promising new biomarker for atherosclerotic and metabolic diseases.
TL;DR: Evidence of increased prooxidant level associated with decreased protective, antioxidative factors suggests their mutual involvement in this complex pathology.
TL;DR: Growing evidence for a role of HDL in glucose metabolism is discussed and the implications of glucoregulatory mechanisms linked to HDL extend from glycemic control to potential anti-ischemic actions via increased tissue glucose uptake and utilization.
Abstract: High-density lipoprotein (HDL) and its principal apolipoprotein A-I (ApoA-I) have now been convincingly shown to influence glucose metabolism through multiple mechanisms. The key clinically relevant observations are that both acute HDL elevation via short-term reconstituted HDL (rHDL) infusion and chronically raising HDL via a cholesteryl ester transfer protein (CETP) inhibitor reduce blood glucose in individuals with type 2 diabetes mellitus (T2DM). HDL may mediate effects on glucose metabolism through actions in multiple organs (e.g., pancreas, skeletal muscle, heart, adipose, liver, brain) by three distinct mechanisms: (i) Insulin secretion from pancreatic beta cells, (ii) Insulin-independent glucose uptake, (iii) Insulin sensitivity. The molecular mechanisms appear to involve both direct HDL signaling actions as well as effects secondary to lipid removal from cells. The implications of glucoregulatory mechanisms linked to HDL extend from glycemic control to potential anti-ischemic actions via increased tissue glucose uptake and utilization. Such effects not only have implications for the prevention and management of diabetes, but also for ischemic vascular diseases including angina pectoris, intermittent claudication, cerebral ischemia and even some forms of dementia. This review will discuss the growing evidence for a role of HDL in glucose metabolism and outline related potential for HDL therapies.
TL;DR: In subjects with atopy and asthma, serum levels of apoA-I and large HDLNMR particles are positively correlated with FEV1, whereas serum triglycerides, LDL cholesterol, and apoB are associated with more severe airflow obstruction.
Abstract: Rationale: Although lipids, apolipoproteins, and lipoprotein particles are important modulators of inflammation, varying relationships exist between these parameters and asthma.Objectives: To determine whether serum lipids and apolipoproteins correlate with the severity of airflow obstruction in subjects with atopy and asthma.Methods: Serum samples were obtained from 154 atopic and nonatopic subjects without asthma, and 159 subjects with atopy and asthma. Serum lipid and lipoprotein levels were quantified using standard diagnostic assays and nuclear magnetic resonance (NMR) spectroscopy. Airflow obstruction was assessed by FEV1% predicted.Measurements and Main Results: Serum lipid levels correlated with FEV1 only in the subjects with atopy and asthma. Serum levels of high-density lipoprotein (HDL) cholesterol and apolipoprotein A-I (apoA-I) were positively correlated with FEV1 in subjects with atopy and asthma, whereas a negative correlation existed between FEV1 and serum levels of triglycerides, low-dens...
TL;DR: Results of the present study clearly demonstrated that treatment with EGCG prior to F intoxication has a significant role in protecting F-induced cardiotoxicity and dyslipidemia in rats.
TL;DR: In Inherited HDL disorders are rare monogenic diseases due to mutations in genes encoding proteins involved in HDL metabolism, and thus represent a unique tool to understand the relationship between plasma HDL concentration, HDL function, and HDL-mediated atheroprotection.
TL;DR: The TG to HDL-C ratio is a powerful independent predictor of all-cause mortality and is a risk factor of cardiovascular events.
Abstract: Aims
High triglycerides (TG) and low high-density lipoprotein cholesterol (HDL-C) are cardiovascular risk factors. A positive correlation between elevated TG/HDL-C ratio and all-cause mortality and cardiovascular events exists in women. However, utility of TG to HDL-C ratio for prediction is unknown among acute coronary syndrome (ACS).
TL;DR: The inhibition of ABCA1 protein degradation by IMM-H007 promotes HDL cholesterol efflux capacity and RCT and attenuates atherogenesis, and potentially represents a lead compound for the development of agents to augment HDL function.
TL;DR: The ‘HDL flux hypothesis’ that therapeutic intervention that targets macrophage cholesterol efflux and RCT may reduce risk is presented, and preclinical studies of such interventions show promise and early phase clinical studies, though small, are encouraging.
Abstract: Purpose of reviewA low level of plasma high density lipoprotein cholesterol (HDL-C) is a strong and independent risk factor for atherosclerotic cardiovascular disease (ASCVD). However, several large studies recently revealed that pharmacologic interventions that increase HDL-C concentration have not
TL;DR: The present study was conducted to gain further understanding of the mechanism(s) responsible for the low HDL‐C levels in patients with CKD and to separate the impact of HD from that of the underlying CKD.
Abstract: Objectives
It has been suggested that a low plasma high-density lipoprotein cholesterol (HDL-C) level contributes to the high cardiovascular disease risk of patients with chronic kidney disease (CKD), especially those undergoing haemodialysis (HD). The present study was conducted to gain further understanding of the mechanism(s) responsible for the low HDL-C levels in patients with CKD and to separate the impact of HD from that of the underlying CKD.
Methods
Plasma lipids and lipoproteins, HDL subclasses and various cholesterol esterification parameters were measured in a total of 248 patients with CKD, 198 of whom were undergoing HD treatment and 40 healthy subjects.
Results
Chronic kidney disease was found to be associated with highly significant reductions in plasma HDL-C, unesterified cholesterol, apolipoprotein (apo)A-I, apoA-II and LpA-I:A-II levels in both CKD cohorts (with and without HD treatment). The cholesterol esterification process was markedly impaired, as indicated by reductions in plasma lecithin:cholesterol acyltransferase (LCAT) concentration and activity and cholesterol esterification rate, and by an increase in the plasma preβ-HDL content. HD treatment was associated with a further lowering of HDL levels and impaired plasma cholesterol esterification. The plasma HDL-C level was highly significantly correlated with LCAT concentration (R = 0.438, P < 0.001), LCAT activity (R = 0.243, P < 0.001) and cholesterol esterification rate (R = 0.149, P = 0.031). Highly significant correlations were also found between plasma LCAT concentration and levels of apoA-I (R = 0.432, P < 0.001), apoA-II (R = 0.275, P < 0.001), LpA-I (R = 0.326, P < 0.001) and LpA-I:A-II (R = 0.346, P < 0.001).
Conclusion
Acquired LCAT deficiency is a major cause of low plasma HDL levels in patients with CKD, thus LCAT is an attractive target for therapeutic intervention to reverse dyslipidaemia, and possibly lower the cardiovascular disease risk in these patients.
TL;DR: It is shown that statins can significantly alter the protein composition of both LDL and HDL and a novel functional relationship between A1AT and HDL is revealed, which enhances its anti-inflammatory functionality and may contribute to the non-lipid lowering beneficial effects of statins.
TL;DR: The increased levels of small, dense LDL3 and LDL4 in NASH may help to at least partly explain the increased risk for atherosclerosis and cardiovascular diseases in patients with NAFLD.
TL;DR: Small peptides that mimic some of the properties of apo A‐I have been shown in pre‐clinical models to improve HDL function and reduce atherosclerosis without altering HDL cholesterol levels.
Abstract: High density lipoprotein (HDL) has long been considered a protective factor against the development of coronary heart disease. Two important roles of HDL include reverse cholesterol transport (RCT) and the modulation of inflammation. The main protein component of HDL; apolipoprotein A-I (apo A-I) is primarily responsible for RCT. Apo A-I can be damaged by oxidative mechanisms, which reduce the protein's ability to promote RCT. In disease states such as diabetes, associated with a chronic acute-phase response, HDL has been found to be dysfunctional and pro-inflammatory. HDL cholesterol levels do not predict composition and/or function and therefore it is important to evaluate the quality and not just the quantity of HDL cholesterol when considering the risk of cardiovascular events. In clinical practice, there are currently no widely available tests for measuring the composition, functionality, and inflammatory properties of HDL. Small peptides that mimic some of the properties of apo A-I have been shown in pre-clinical models to improve HDL function and reduce atherosclerosis without altering HDL cholesterol levels. Clinical trials using HDL and HDL mimetics as therapeutic agents are currently underway. Results in animal studies and early clinical trials will be reviewed.
TL;DR: This study demonstrates that the elevated TG/HDL-C ratio predicts poor CVD outcome in subjects with CKD and may emerge as a novel and reliable indicator among the many well-established markers of CVD risk in CKD.
Abstract: Background
Cardiovascular disease (CVD) risk is substantially increased in subjects with chronic kidney disease (CKD). The Triglycerides (TG) to High-Density Lipoprotein Cholesterol (HDL-C) ratio is an indirect measure of insulin resistance and an independent predictor of cardiovascular risk. No study to date has been performed to evaluate whether the TG/HDL-C ratio predicts CVD risk in patients with CKD.
TL;DR: The substitution of fatty acids (FA) for carbohydrates is beneficially associated with HDL metabolism, and trans-FA is significantly associated with reduction of HDL-C, and is also adversely related with total cholesterol/HDL-C.
Abstract: High-density lipoprotein (HDL) is a lipoprotein which has anti-atherogenic property by reversing cholesterol transport from the peripheral tissues to liver. Low HDL-cholesterol (HDL-C) as well as high low-density lipoprotein-cholesterol (LDL-C) is associated with the development of coronary heart diseases (CHD). Various epidemiological studies have suggested that the development of CHD increase in individuals with less than 40 mg/dL of HDL-C. In spite of accumulation of evidences suggesting a significant association between low HDL-C and CHD, effects of dietary factors on HDL metabolism remained largely unknown. We reviewed published articles about effects of dietary fat intake on HDL metabolism. The substitution of fatty acids (FA) for carbohydrates is beneficially associated with HDL metabolism. Monounsaturated FA intake may not affect HDL-C. Trans-FA is significantly associated with reduction of HDL-C, and is also adversely related with total cholesterol/HDL-C. Fish oils consumption, especially docosahexaenoic acid consumption, may be favorably associated with HDL metabolism. Although plant sterols and stanols may not affect HDL-C, policosanol intake is associated with a clinically significant decrease in the LDL/HDL ratio.
TL;DR: Observations indicate that the HDL proteome is extensively remodeled in uremic subjects, and alterations of the protein cargo of HDL might impact HDL's proposed cardioprotective properties.
Abstract: Cardiovascular disease is the leading cause of death in end-stage renal disease (ESRD) patients treated with hemodialysis. An important contributor might be a decline in the cardioprotective effects of high-density lipoprotein (HDL). One important factor affecting HDL’s cardioprotective properties may involve the alterations of protein composition in HDL. In the current study, we used complementary proteomics approaches to detect and quantify relative levels of proteins in HDL isolated from control and ESRD subjects. Shotgun proteomics analysis of HDL isolated from 20 control and 40 ESRD subjects identified 63 proteins in HDL. Targeted quantitative proteomics by isotope-dilution selective reaction monitoring revealed that 22 proteins were significantly enriched and 6 proteins were significantly decreased in ESRD patients. Strikingly, six proteins implicated in renal disease, including B2M, CST3, and PTGDS, were markedly increased in HDL of uremic subjects. Moreover, several of these proteins (SAA1, apoC-III, PON1, etc.) have been associated with atherosclerosis. Our observations indicate that the HDL proteome is extensively remodeled in uremic subjects. Alterations of the protein cargo of HDL might impact HDL’s proposed cardioprotective properties. Quantifying proteins in HDL may be useful in the assessment of cardiovascular risk in patients with ESRD and in assessing response to therapeutic interventions.