Atherogenic lipoprotein phenotype in end-stage renal failure: Origin and extent of small dense low-density lipoprotein formation

2000 ◽  
Vol 35 (5) ◽  
pp. 852-862 ◽  
Author(s):  
Christopher J. Deighan ◽  
Muriel J. Caslake ◽  
Michael McConnell ◽  
J.Michael Boulton-Jones ◽  
Christopher J. Packard
Keyword(s):  
Renal Failure ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
End Stage Renal Failure ◽  
Atherogenic Lipoprotein ◽  
Atherogenic Lipoprotein Phenotype ◽  
End Stage ◽  
Lipoprotein Phenotype

Oxidized Low-Density Lipoprotein Biomarkers in Patients with End-Stage Renal Failure: Acute Effects of Hemodialysis

2007 ◽  
Vol 25 (5-6) ◽  
pp. 457-465 ◽  
Author(s):  
Maurizio Bossola ◽  
Luigi Tazza ◽  
Esther Merki ◽  
Stefania Giungi ◽  
Giovanna Luciani ◽  
...  
Keyword(s):  
Renal Failure ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Acute Effects ◽  
Oxidized Low Density Lipoprotein ◽  
End Stage Renal Failure ◽  
End Stage

Effects of hemodialysis and vitamin E supplementation on low-density lipoprotein oxidizability in end-stage renal failure

2012 ◽  
Vol 26 (3) ◽  
pp. 549-555 ◽  
Author(s):  
Simona Baldi ◽  
Maurizio Innocenti ◽  
Silvia Frascerra ◽  
Monica Nannipieri ◽  
Alberto Lippi ◽  
...  
Keyword(s):  
Renal Failure ◽  
Vitamin E ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
End Stage Renal Failure ◽  
End Stage ◽  
Vitamin E Supplementation

scholarly journals Comparative Effects of Cerivastatin and Fenofibrate on the Atherogenic Lipoprotein Phenotype in Proteinuric Renal Disease

2001 ◽  
Vol 12 (2) ◽  
pp. 341-348
Author(s):  
CHRISTOPHER J. DEIGHAN ◽  
MURIEL J. CASLAKE ◽  
MICHAEL MCCONNELL ◽  
J. MICHAEL BOULTON-JONES ◽  
CHRISTOPHER J. PACKARD
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
High Density Lipoproteins ◽  
Low Density ◽  
Atherogenic Lipoprotein ◽  
Fenofibrate Treatment ◽  
Remnant Lipoproteins ◽  
Atherogenic Lipoprotein Phenotype ◽  
Nephrotic Range Proteinuria ◽  
Lipoprotein Phenotype

Abstract. Patients with nephrotic-range proteinuria have impaired clearance of triglyceride-rich lipoproteins. This results in the atherogenic lipoprotein phenotype (mild hypertriglyceridemia, low high-density lipoproteins [HDL], and excess small, dense low-density lipoproteins [LDLIII]). Excess remnant lipoproteins (RLP) are linked to hypertriglyceridemia and may contribute to the atherogenicity of nephrotic dyslipidemia. A randomized crossover study compared the effects of a statin (cerivastatin) and a fibrate (fenofibrate) on LDLIII and RLP in 12 patients with nephrotic-range proteinuria. Cerivastatin reduced cholesterol (21%, P < 0.01), triglyceride (14%, P < 0.05), LDL cholesterol (LDL-C; 23%, P < 0.01), total LDL (18%, P < 0.01), and LDLIII concentration (27% P < 0.01). %LDLIII, RLP-C, and RLP triglyceride (RLP-TG) were unchanged. Plasma LDLIII reduction with cerivastatin treatment correlated with LDL-C reduction (r2 = 34%, P < 0.05). Fenofibrate lowered cholesterol (19%), triglyceride (41%), very low-density lipoprotein cholesterol (52%), LDLIII concentration (49%), RLP-C (35%), and RLP-TG (44%; all P < 0.01). Fenofibrate also reduced %LDLIII from 60 to 33% (P < 0.01). HDL-C (19%, P < 0.01) increased with fenofibrate treatment; LDL-C and total LDL were unchanged. The reduction in LDLIII concentration and RLP-C with fenofibrate treatment correlated with plasma triglyceride reduction (LDLIII r2 = 67%, P < 0.001; RLP cholesterol r2 = 58%, P < 0.005). Serum creatinine increased with fenofibrate treatment (14%, P < 0.01); however, creatinine clearance was unchanged. LDLIII concentration was 187 ± 85 mg/dl after cerivastatin treatment and 133 ± 95 mg/dl after fenofibrate treatment. Cerivastatin and fenofibrate reduce LDLIII concentration in nephrotic-range proteinuria. However, atherogenic concentrations of LDLIII remain prevalent after either treatment. Fenofibrate but not cerivastatin reduces remnant lipoproteins. The two treatments seem to reduce LDLIII by different mechanisms, suggesting a potential role for combination therapy to optimize lowering of LDLIII and RLP.

Inter-relationships between small, dense low-density lipoprotein (LDL), plasma triacylglycerol and LDL apoprotein B in an atherogenic lipoprotein phenotype in free-living subjects

1999 ◽  
Vol 97 (3) ◽  
pp. 269-276 ◽  
Author(s):  
B. A. GRIFFIN ◽  
A. M. MINIHANE ◽  
N. FURLONGER ◽  
C. CHAPMAN ◽  
M. MURPHY ◽  
...  
Keyword(s):  
Particle Number ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Free Living ◽  
Small Dense Ldl ◽  
Atherogenic Lipoprotein ◽  
Apoprotein B ◽  
Plasma Triacylglycerol ◽  
Atherogenic Lipoprotein Phenotype ◽  
Lipoprotein Phenotype

A predominance of small, dense low-density lipoprotein (LDL) is a major component of an atherogenic lipoprotein phenotype, and a common, but modifiable, source of increased risk for coronary heart disease in the free-living population. While much of the atherogenicity of small, dense LDL is known to arise from its structural properties, the extent to which an increase in the number of small, dense LDL particles (hyper-apoprotein B) contributes to this risk of coronary heart disease is currently unknown. This study reports a method for the recruitment of free-living individuals with an atherogenic lipoprotein phenotype for a fish-oil intervention trial, and critically evaluates the relationship between LDL particle number and the predominance of small, dense LDL. In this group, volunteers were selected through local general practices on the basis of a moderately raised plasma triacylglycerol (triglyceride) level (> 1.5 mmol/l) and a low concentration of high-density-lipoprotein cholesterol (< 1.1 mmol/l). The screening of LDL subclasses revealed a predominance of small, dense LDL (LDL subclass pattern B) in 62% of the cohort. As expected, subjects with LDL subclass pattern B were characterized by higher plasma triacylglycerol and lower high-density lipoprotein cholesterol (< 1.1 mmol/l) levels and, less predictably, by lower LDL cholesterol and apoprotein B levels (P < 0.05; LDL subclass A compared with subclass B). While hyper-apoprotein B was detected in only five subjects, the relative percentage of small, dense LDL-III in subjects with subclass B showed an inverse relationship with LDL apoprotein B (r =-0.57; P < 0.001), identifying a subset of individuals with plasma triacylglycerol above 2.5 mmol/l and a low concentration of LDL almost exclusively in a small and dense form. These findings indicate that a predominance of small, dense LDL and hyper-apoprotein B do not always co-exist in free-living groups. Moreover, if coronary risk increases with increasing LDL particle number, these results imply that the risk arising from a predominance of small, dense LDL may actually be reduced in certain cases when plasma triacylglycerol exceeds 2.5 mmol/l.

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