The mechanism of hyperlipidaemia in the nephrotic syndrome.
The mechanism of hyperlipidaemia in the nephrotic syndrome has not been fully established. We propose that it results from hypoalbuminaemia due to inhibition of the reaction catalysed by lecithin cholesterol acyltransferase converting cholesterol of high density lipoproteins to cholesterol esters and to an inhibition of high density lipoprotein particle formation from very low density lipoproteins due to reduced activity of lipoprotein lipase.
D002648:Child; D002784:Cholesterol / Q000378:metabolism; D002788:Cholesterol Esters / Q000096:biosynthesis; D006801:Humans; D006937:Hypercholesterolemia / Q000209:etiology; D006949:Hyperlipidemias / Q000209:etiology*; D008071:Lipoprotein Lipase / Q000378:metabolism; D008075:Lipoproteins, HDL / Q000096:biosynthesis; D009402:Nephrosis, Lipoid / Q000150:complications; D009404:Nephrotic Syndrome / Q000150:complications* / Q000378:metabolism; D007862:Phosphatidylcholine-Sterol O-Acyltransferase / Q000378:metabolism; D012709:Serum Albumin / Q000378:metabolism*
D002788:Cholesterol Esters; D008075:Lipoproteins, HDL; D012709:Serum Albumin; D002784:Cholesterol; D007862:Phosphatidylcholine-Sterol O-Acyltransferase; D008071:Lipoprotein Lipase