Lipoprotein Metabolism and Renal Failure

Attman, Per-Ola; Samuelsson, Ola; Alaupovic, Petar

doi:10.1016/s0272-6386(12)80030-8

Cited by 326 publications

(247 citation statements)

References 151 publications

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“…This is in accordance with other reports, which show that patients with end-stage renal disease have low levels of HDL-C and increased levels of very-low density lipoprotein (VLDL) and intermediate-density lipoprotein (IDL), leading to elevated triglyceride levels. 22,23 We also found that in the PD group, patients have higher cholesterol and Apo-B levels than in HD group, as reported previously. 7,24,25 A possible explanation for this abnormality is the exposure of patients to glucose in the dialysate and insulin resistance that activates the delivery of free fatty acids (FFAs) to the liver and subsequently the oxidation or esterification of FFAs to cytosolic triglycerides or VLDL.…”

Section: Discussionsupporting

confidence: 88%

Lipid Abnormalities and Oxidized LDL in Chronic Kidney Disease Patients on Hemodialysis and Peritoneal Dialysis

et al. 2011

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Dyslipoproteinemia and oxidative modification of low-density lipoprotein (oxLDL) contribute to the development of oxidative stress and atherosclerosis in chronic kidney disease (CKD). On the contrary, high-density lipoprotein cholesterol (HDL-C), especially HDL3-C subtype, has protective effect against oxidative damage. There is limited evidence referring HDL-C subclass levels in patients on dialysis. This study was designed to compare lipid abnormalities and oxLDL levels in hemodialysis (HD) and peritoneal dialysis (PD) patients. Serum lipids, HDL subclasses, and oxLDL were measured in 55 patients with CKD-stage 5 (31 patients on HD and 24 patients on PD) and in 21 normal controls (NC). The results showed that in dialysis patients, triglycerides were higher than in controls (p < 0.0001) and HDL-C was significantly lower (p < 0.0001). The HDL2-C subclass concentration did not differ significantly between patients and controls, while HDL3-C was lower in patients (11 ± 0.5 mg/dL) than in NC (23 ± 1, p < 0.0001). oxLDL levels were markedly increased in patients (1.92 ± 0.29 mg/L) compared to NC (0.22 ± 0.05, p < 0.0001). Patients on PD had higher levels of cholesterol (p < 0.001) and apolipoprotein B (p < 0.05) than patients on HD. However, HDL-C, HDL-C subclasses, and oxLDL concentrations did not differ significantly between PD and HD patients. It is concluded that patients with CKD have a nearly 10-fold elevation of oxLDL compared with NC. Patients on PD have differences in the lipid profile compared with patients on HD; however, both modalities seem to possess similar potential to atherosclerosis development.

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Section: Discussionsupporting

confidence: 88%

Lipid Abnormalities and Oxidized LDL in Chronic Kidney Disease Patients on Hemodialysis and Peritoneal Dialysis

et al. 2011

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“…A beneficial effect of PTX on cholesterol levels had been observed by Shigematsu et al (9) and numerous other authors (57)(58)(59)(60)(61), but the effect of PTH is probably independent of the presence or absence of renal failure as suggested by the observation of reversible hyperlipoproteinemia in patients with primary hyperparathyroidism (58). This was associated with a decrease in post-heparin LPL activity (60).…”

Section: Discussionmentioning

confidence: 86%

Beneficial Effects of Calcimimetics on Progression of Renal Failure and Cardiovascular Risk Factors

Ogata¹,

Ritz²,

Odoni³

et al. 2003

Journal of the American Society of Nephrology

137

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Abstract. In renal failure, parathyroid hormone (PTH) is not only involved in the genesis of disturbed calcium/phosphate metabolism and ostitis fibrosa; it is also a permissive factor in the genesis of hypertension, cardiovascular damage, and dyslipidemia. The allosteric activator of the calcium sensing receptor NPSR-568 (R-568) has been shown to reduce the serum intact PTH (iPTH) concentration in uremic rats. It was the purpose of this study in subtotally nephrectomized (SNX) rats to compare pharmacologic abrogation of secondary hyperparathyroidism by R-568 with parathyroidectomy (PTX). The effects on progression of renal failure, BP, and lipid and structural parameters of kidney and heart were studied. Four groups of male SD-rats were studied: (1) sham-operated ϩ vehicletreated rats (controls); (2) SNX ϩ vehicle-treated rats (SNX); (3) parathyroidectomized SNX ϩ vehicle-treated rats (SNXϩPTX); and (4) SNX ϩ calcimimetic R-568 -treated rats (SNXϩR-568). R-568 (50 mol/kg per d) was administered by gavage. Eight weeks after SNX, serum creatinine concentration, urinary albumin excretion, BP, and serum LDL-cholesterol concentration were significantly lower in both R-568 -treated and parathyroidectomized SNX compared with vehicletreated SNX. In addition, structural abnormalities of the kidney (glomerulosclerosis, tubulointerstitial changes) and the heart (interstitial fibrosis, capillary length density, arteriolar wall thickness) were significantly less pronounced than in vehicletreated SNX. It is concluded that in experimental renal failure abrogation of hyperparathyroidism by administration of a calcimimetic or PTX similarly attenuates progression of renal failure. Furthermore, it interferes with the development of cardiovascular risk factors and cardiac remodeling.Secondary hyperparathyroidism (sHPT) is a known complication of chronic renal failure. Elevated concentrations of parathyroid hormone (PTH) play a role not only in the pathogenesis of renal bone disease (1,2), but also in the development of cardiovascular risk factors such as disturbed lipid metabolism (3,4), glucose intolerance (5), and hypertension (6 -8). Parathyroidectomy (PTX) attenuates progression of renal failure in subtotally nephrectomized rats (SNX) on a high protein (9) or high phosphate (10,11) diet. sHPT is also known to play an important role in the development of structural abnormalities of the heart in renal failure, including left ventricular hypertrophy, interstitial fibrosis, and arteriolar wall thickening of the heart (7,(12)(13)(14).Allosteric activators of the calcium sensing receptor, e.g., NPSR-568 (R-568), reduce PTH secretion in rats or patients with primary and secondary hyperparathyroidism (15-20).There is no information on whether calcimimetics also affect abnormalities of uremia other than calcemia, phosphatemia (21), PTH concentrations (22), and skeletal abnormalities (17).Therefore, it was the purpose of this study to compare the effects of the calcimimetic R-568 and of parathyroidectomy on progression of renal failure, ...

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“…However, low-density-lipoprotein (LDL) cholesterol values were found to be within normal limits or reduced in this population. 7 Epicardial adipose tissue (EAT) originates from the splanchnopleuric mesoderm. 8 Mazurek et al 9 concluded that, like abdominal visceral adipose tissue, EAT is also metabolically active because it can secrete proinflammatory cytokines and utilize free fatty acids (FFAs).…”

Section: Introductionmentioning

confidence: 99%

The relationship between atherogenic index of plasma and epicardial adipose tissue in hemodialysis and peritoneal dialysis patients

Erdur¹,

Tonbul²,

Özbiner

et al. 2013

Renal Failure

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Lipoprotein Metabolism and Renal Failure

Cited by 326 publications

References 151 publications

Lipid Abnormalities and Oxidized LDL in Chronic Kidney Disease Patients on Hemodialysis and Peritoneal Dialysis

Lipid Abnormalities and Oxidized LDL in Chronic Kidney Disease Patients on Hemodialysis and Peritoneal Dialysis

Beneficial Effects of Calcimimetics on Progression of Renal Failure and Cardiovascular Risk Factors

The relationship between atherogenic index of plasma and epicardial adipose tissue in hemodialysis and peritoneal dialysis patients

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