Lipoprotein distribution and composition in the human nephrotic syndrom

Muls, Erik; Rosseneu, Maryvonne; Daneels, R; Schurgers, M.; Boelaert, Johan R.

doi:10.1016/0021-9150(85)90181-9

Cited by 73 publications

(32 citation statements)

References 32 publications

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“…In contrast to the study done by El-Melegy et al, who found lower levels of HDL in cases, we found no significant differences in the mean levels of HDL between Group 1 and Group 2 [1]. This is in accordance to study done by Muls et al, who found normal levels of HDL in NS [20]. They also reported abnormal distribution of HDL subtypes.…”

Section: Discussionsupporting

confidence: 80%

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Paraoxonase Activity and Lipid Profile in Paediatric Nephrotic Syndrome: A Cross-sectional Study

Patil

et al. 2016

JCDR

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Section: Discussionsupporting

confidence: 80%

“…Also, Hu P et al, observed higher levels of HDL in nephrotic cases compared to controls [19]. There is increased levels of HDL 3 and decreased HDL 2 [20][21][22] which measured together give normal values for total HDL, but result in defective reverse cholesterol transport pathway.…”

Section: Discussionmentioning

confidence: 96%

Paraoxonase Activity and Lipid Profile in Paediatric Nephrotic Syndrome: A Cross-sectional Study

Patil

et al. 2016

JCDR

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“…47 Maturation of HDL-3 to HDL-2 is impaired in NS. [1][2][3][4]14 This is because of acquired LCAT deficiency, which was nearly corrected by ACAT inhibitor.…”

Section: Discussionmentioning

confidence: 99%

Acyl-Coenzyme A:Cholesterol Acyltransferase Inhibition Ameliorates Proteinuria, Hyperlipidemia, Lecithin-Cholesterol Acyltransferase, SRB-1, and Low-Denisty Lipoprotein Receptor Deficiencies in Nephrotic Syndrome

Vaziri

Liang

2004

Circulation

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Background-Nephrotic syndrome (NS) is associated with hyperlipidemia, altered lipid regulatory enzymes and receptors, and increased risk of progressive renal and cardiovascular diseases. Acyl-coenzyme A:cholesterol acyltransferase (ACAT) catalyzes intracellular esterification of cholesterol and plays an important role in production of apolipoprotein B-containing lipoproteins, regulation of cholesterol-responsive proteins, and formation of foam cells. Because hepatic ACAT-2 is markedly upregulated in NS, we tested the hypothesis that inhibition of ACAT may improve cholesterol metabolism in NS. Methods and Results-Rats with puromycin-induced NS were treated with either the ACAT inhibitor CI-976 or placebo for 2 weeks. Normal rats served as controls. Plasma lipids, renal function, and key lipid regulatory factors were measured. Untreated NS rats showed heavy proteinuria; hypoalbuminemia; elevated plasma cholesterol, triglyceride, LDL, VLDL, and total cholesterol-to-HDL cholesterol ratio; increased hepatic ACAT activity, ACAT-2 mRNA, and ACAT-2 protein; and reduced LDL receptor, HDL receptor, otherwise known as scavenger receptor B-1 (SRB-1) and plasma lecithin-cholesterol acyltransferase (LCAT). ACAT inhibitor reduced plasma cholesterol and triglycerides, normalized total cholesterol-to-HDL cholesterol ratio, and lowered hepatic ACAT activity without changing ACAT-2 mRNA or protein. This was accompanied by near normalizations of plasma LCAT, hepatic SRB-1, and LDL receptor and a significant amelioration of proteinuria and hypoalbuminemia. Conclusions-Pharmacological

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“…Furthermore, the maturation of cholesterol ester-poor HDL 3 to cholesterol esterrich HDL 2 is often impaired in these patients, which leads to an increase in HDL 3 and a decrease in HDL 2 in the circulation 33 . This phenomenon is indicative of impaired HDL-mediated reverse cholesterol transport and can, in part, account for the pro-atherogenic effects of proteinuria.…”

Section: Abnormalities Of Hdl Metabolismmentioning

confidence: 99%

HDL abnormalities in nephrotic syndrome and chronic kidney disease

2015

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| Normal HDL activity confers cardiovascular and overall protection by mediating reverse cholesterol transport and through its potent anti-inflammatory, antioxidant, and antithrombotic functions. Serum lipid profile, as well as various aspects of HDL metabolism, structure, and function can be profoundly altered in patients with nephrotic range proteinuria or chronic kidney disease (CKD). These abnormalities can, in turn, contribute to the progression of cardiovascular complications and various other comorbidities, such as foam cell formation, atherosclerosis, and/or glomerulosclerosis, in affected patients. The presence and severity of proteinuria and renal insufficiency, as well as dietary and drug regimens, pre-existing genetic disorders of lipid metabolism, and renal replacement therapies (including haemodialysis, peritoneal dialysis, and renal transplantation) determine the natural history of lipid disorders in patients with kidney disease. Despite the adverse effects associated with dysregulated reverse cholesterol transport and advances in our understanding of the underlying mechanisms, safe and effective therapeutic interventions are currently lacking. This Review provides an overview of HDL metabolism under normal conditions, and discusses the features, mechanisms, and consequences of HDL abnormalities in patients with nephrotic syndrome or advanced CKD.

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Lipoprotein distribution and composition in the human nephrotic syndrom

Cited by 73 publications

References 32 publications

Paraoxonase Activity and Lipid Profile in Paediatric Nephrotic Syndrome: A Cross-sectional Study

Paraoxonase Activity and Lipid Profile in Paediatric Nephrotic Syndrome: A Cross-sectional Study

Acyl-Coenzyme A:Cholesterol Acyltransferase Inhibition Ameliorates Proteinuria, Hyperlipidemia, Lecithin-Cholesterol Acyltransferase, SRB-1, and Low-Denisty Lipoprotein Receptor Deficiencies in Nephrotic Syndrome

HDL abnormalities in nephrotic syndrome and chronic kidney disease

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