Analysis of cardiovascular risk factors in chronic hemodialysis patients with special attention to the hyperlipoproteinemias

Hahn, R.; Oette, K.; Mondorf, H.; Finke, K.; Sieberth, H. G.

doi:10.1016/0021-9150(83)90045-x

Cited by 95 publications

(35 citation statements)

References 16 publications

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“…The present study confirms previously well-known lipid anomalies in ufaemic patients treated or untreated by intermittent haemodialysis, i. e., hypertriglyceridaemia, a decrease of serum HDL-cholesterol and an increase of the so-called cardiovascular risk factors (13,15,16,(18)(19)(20)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38). In addition, we have demonstrated that lipid anomalies were more marked in uraemic patients with more advanced renal failure than in those with moderate renal insufficiency.…”

Section: Discussionsupporting

confidence: 90%

Comparison of Several Atherogenicity Indices by the Analysis of Serum Lipoprotein Composition in Patients with Chronic Renal Failure with or without Haemodialysis, and in Renal Transplant Patients

Lacour

Roullet

Beyne

et al. 1985

Clinical Chemistry and Laboratory Medicine

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Section: Discussionsupporting

confidence: 90%

Comparison of Several Atherogenicity Indices by the Analysis of Serum Lipoprotein Composition in Patients with Chronic Renal Failure with or without Haemodialysis, and in Renal Transplant Patients

Lacour

Roullet

Beyne

et al. 1985

Clinical Chemistry and Laboratory Medicine

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“…Diabetics suffer from high rates of coronary heart disease (CHD), and the rates climb even higher in those with diabetic nephropathy [1][2][3] . A recent prospective cohort study of patients with type 2 diabetes mellitus has demonstrated that diabetic nephropathy is significantly associated with subsequent mortality from CHD even before end-stage renal disease (ESRD) 4) .…”

Section: Introductionmentioning

confidence: 99%

Significant Increase of Apolipoprotein B48 Levels by a Standard Test Meal in Type 2 Diabetic Patients with Nephropathy

Yamamoto

Hirano

Mori

et al. 2008

JAT

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Aim:We investigated postprandial changes of apolipoprotein (apo) B48 in type 2 diabetics at different stages of diabetic nephropathy in order to explore non-traditional lipid abnormalities in diabetic nephropathy. Methods: Twenty-two healthy controls and 56 type 2 diabetics with normoalbuminuria (NA), microalbuminuria (MA), and overt albuminuria (OA) were enrolled. Blood samples were taken at 0, 1, 2, 4, 6 h after the ingestion of Test meal A (460 Kcal, 18 g fat). The maximal increase of triglyceride (TG) was 40% above baseline in controls and 17% above baseline in diabetics. The incremental area under the curve (iAUC) of TG, however, was comparable among controls and diabetics with NA, MA, and OA. The maximal increase of apoB48 was 92% above baseline in controls and 56-88% above baseline in diabetics. Apo B48-iAUC was significantly higher in diabetics than in controls, and diabetics with OA exhibited the highest apoB48-iAUC among the diabetic subgroups. Small dense low-density lipoprotein-cholesterol (LDL-C) was elevated in diabetic nephropathy, and apoB48-iAUC was positively associated with the level of sd-LDL-C. Conclusions: ApoB48 is a sensitive marker for postprandial lipemia, a condition which is significantly increased in diabetic nephropathy and associated with an increase of potent atherogenic sd-LDL particles. J Atheroscler

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“…This abnormality is largely due to marked downregulation of lecithin:cholesterol acyltransferase (LCAT) (12, 23, 33), which is essential for optimal cholesterol uptake by HDL. The CRF-induced abnormalities of triglyceride-rich lipoprotein metabolism are manifested by hypertriglyceridemia, elevated level and impaired clearance of very-low-density lipoprotein (VLDL), increased plasma intermediate-density lipoprotein (IDL) concentration, and depressed clearance of chylomicrons (2,7,13,26,27). These abnormalities are primarily due to downregulation of adipose tissue and skeletal muscle lipoprotein lipase (29,36) and VLDL receptor (20, 30), as well as hepatic triglyceride lipase deficiency (16).…”

mentioning

confidence: 99%

“…The atherogenic diathesis in this population is, in part, due to profound abnormalities of high-density lipoprotein (HDL) and triglyceride-rich Apo-B-containing lipoproteins (2,7,13,27). The CRF-associated HDL abnormalities are marked by a reduction of plasma HDL cholesterol relative to the non-HDL cholesterol concentration and impaired maturation of cholesterol ester-poor HDL-3 to cholesterol ester-rich cardioprotective HDL-2 (2,27).…”

mentioning

confidence: 99%

ACAT inhibition reverses LCAT deficiency and improves plasma HDL in chronic renal failure

Vaziri¹,

Liang²

2004

American Journal of Physiology-Renal Physiology

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Vaziri, N. D., and K. Liang. ACAT inhibition reverses LCAT deficiency and improves plasma HDL in chronic renal failure. Am J Physiol Renal Physiol 287: F1038 -F1043, 2004. First published July 27, 2004 doi:10.1152/ajprenal.00150.2004.-Chronic renal failure (CRF) is associated with increased risk of arteriosclerotic cardiovascular disease and profound alteration of plasma lipid profile. Uremic dyslipidemia is marked by increased plasma concentration of ApoBcontaining lipoproteins and impaired high-density lipoprotein (HDL)-mediated reverse cholesterol transport. These abnormalities are, in part, due to acquired LCAT deficiency and upregulation of hepatic acyl-CoA:cholesterol acyltransferase (ACAT). ACAT catalyzes intracellular esterification of cholesterol, thereby promoting hepatic production of ApoB-containing lipoproteins and constraining HDL-mediated cholesterol uptake in the peripheral tissues. In view of the above considerations, we tested the hypothesis that pharmacological inhibition of ACAT may ameliorate CRF-induced dyslipidemia. 5/6 Nephrectomized rats were treated with either ACAT inhibitor IC-976 (30 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 ) or placebo for 6 wk. Sham-operated rats served as controls. Key cholesterol-regulating enzymes, plasma lipids, and creatinine clearance were measured. The untreated CRF rats exhibited increased plasma low-density lipoprotein (LDL) and very LDL (VLDL) cholesterol, unchanged plasma HDL cholesterol, elevated total cholesterol-to-HDL cholesterol ratio, reduced liver microsomal free cholesterol, and diminished creatinine clearance. This was accompanied by reduced plasma LCAT, increased hepatic ACAT-2 mRNA, ACAT-2 protein and ACAT activity, and unchanged hepatic HMG-CoA reductase and cholesterol 7␣-hydroxylase. ACAT inhibitor raised plasma HDL cholesterol, lowered LDL and VLDL cholesterol, and normalized total cholesterol-to-HDL cholesterol ratio without changing total cholesterol concentration (hence, a shift from ApoB-containing lipoproteins to HDL). This was accompanied by normalizations of hepatic ACAT activity and plasma LCAT. In conclusion, inhibition of ACAT reversed LCAT deficiency and improved plasma HDL level in CRF rats. Future studies are needed to explore the efficacy of ACAT inhibition in humans with CRF.high-density lipoprotein; hyperlipidemia; lecithin:cholesterol acyltransferase; cholesterol; acyl-CoA:cholesterol acyltransferase; progression of renal disease; atherosclerosis; cardiovascular disease; end-stage renal disease ACCELERATED ATHEROSCLEROTIC cardiovascular disease is a major complication of chronic renal failure (CRF) and the main cause of mortality among dialysis-dependent and dialysis-independent patients (3, 10). The atherogenic diathesis in this population is, in part, due to profound abnormalities of high-density lipoprotein (HDL) and triglyceride-rich Apo-B-containing lipoproteins (2, 7, 13, 27). The CRF-associated HDL abnormalities are marked by a reduction of plasma HDL cholesterol relative to the non-HDL cholesterol concentration and impaired maturation...

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Analysis of cardiovascular risk factors in chronic hemodialysis patients with special attention to the hyperlipoproteinemias

Cited by 95 publications

References 16 publications

Comparison of Several Atherogenicity Indices by the Analysis of Serum Lipoprotein Composition in Patients with Chronic Renal Failure with or without Haemodialysis, and in Renal Transplant Patients

Comparison of Several Atherogenicity Indices by the Analysis of Serum Lipoprotein Composition in Patients with Chronic Renal Failure with or without Haemodialysis, and in Renal Transplant Patients

Significant Increase of Apolipoprotein B48 Levels by a Standard Test Meal in Type 2 Diabetic Patients with Nephropathy

ACAT inhibition reverses LCAT deficiency and improves plasma HDL in chronic renal failure

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