Dyslipidemia in chronic kidney disease: Causes and consequences
Cardiovascular risk increases with each decrement in renal function. Abnormalities in plasma lipoprotein composition among patients with end-stage renal disease represent a change both in lipoprotein level and structure. Low-density lipoprotein (LDL) cholesterol is not increased and LDL level is not...
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Published in | Kidney international Vol. 70; no. S104; pp. S55 - S58 |
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Main Author | |
Format | Journal Article |
Language | English |
Published |
London
Elsevier Inc
01.12.2006
Elsevier Limited |
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Abstract | Cardiovascular risk increases with each decrement in renal function. Abnormalities in plasma lipoprotein composition among patients with end-stage renal disease represent a change both in lipoprotein level and structure. Low-density lipoprotein (LDL) cholesterol is not increased and LDL level is not strongly correlated with outcome. In contrast, high-density lipoprotein (HDL) levels are decreased and are inversely associated with cardiovascular risk. HDL is decreased because of an increased rate of catabolism associated with a predominance of small dense HDL. HDL fails to mature normally as a result of decreased lecithin cholesterol ester (CE) transfer protein (lecithin:cholesterol acyltransferase), leaving CE poor, triglyceride (TG) rich HDL3, and pre β HDL. Chronic kidney disease (CKD) also causes insulin resistance, and this may also contribute to low HDL levels. Plasma TG levels are increased and TGs are found in an expanded intermediate density lipoprotein (IDL) pool. These are composed of chylomicron and very low-density lipoprotein remnants resulting from delayed lipolysis on the endothelium and impaired hepatic uptake. IDL in contrast to LDL is associated with vascular disease in dialysis patients. Lipoprotein (a) (Lp (a)) levels are also increased. In patients without renal disease. The concentration of Lp (a) is inversely associated with the size of the apolipoprotein (a) isoform inherited; Lp (a) levels are increased in patients with kidney disease as a consequence of increased concentrations, primarily of the high molecular weight isoform. Lp (a) levels are also associated with cardiovascular outcome among dialysis patients. |
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AbstractList | Cardiovascular risk increases with each decrement in renal function. Abnormalities in plasma lipoprotein composition among patients with end-stage renal disease represent a change both in lipoprotein level and structure. Low-density lipoprotein (LDL) cholesterol is not increased and LDL level is not strongly correlated with outcome. In contrast, high-density lipoprotein (HDL) levels are decreased and are inversely associated with cardiovascular risk. HDL is decreased because of an increased rate of catabolism associated with a predominance of small dense HDL. HDL fails to mature normally as a result of decreased lecithin cholesterol ester (CE) transfer protein (lecithin:cholesterol acyltransferase), leaving CE poor, triglyceride (TG) rich HDL3, and pre β HDL. Chronic kidney disease (CKD) also causes insulin resistance, and this may also contribute to low HDL levels. Plasma TG levels are increased and TGs are found in an expanded intermediate density lipoprotein (IDL) pool. These are composed of chylomicron and very low-density lipoprotein remnants resulting from delayed lipolysis on the endothelium and impaired hepatic uptake. IDL in contrast to LDL is associated with vascular disease in dialysis patients. Lipoprotein (a) (Lp (a)) levels are also increased. In patients without renal disease. The concentration of Lp (a) is inversely associated with the size of the apolipoprotein (a) isoform inherited; Lp (a) levels are increased in patients with kidney disease as a consequence of increased concentrations, primarily of the high molecular weight isoform. Lp (a) levels are also associated with cardiovascular outcome among dialysis patients.Kidney International (2006) 70, S55-S58. doi:10.1038/sj.ki.5001979 Cardiovascular risk increases with each decrement in renal function. Abnormalities in plasma lipoprotein composition among patients with end-stage renal disease represent a change both in lipoprotein level and structure. Low-density lipoprotein (LDL) cholesterol is not increased and LDL level is not strongly correlated with outcome. In contrast, high-density lipoprotein (HDL) levels are decreased and are inversely associated with cardiovascular risk. HDL is decreased because of an increased rate of catabolism associated with a predominance of small dense HDL. HDL fails to mature normally as a result of decreased lecithin cholesterol ester (CE) transfer protein (lecithin:cholesterol acyltransferase), leaving CE poor, triglyceride (TG) rich HDL3, and pre β HDL. Chronic kidney disease (CKD) also causes insulin resistance, and this may also contribute to low HDL levels. Plasma TG levels are increased and TGs are found in an expanded intermediate density lipoprotein (IDL) pool. These are composed of chylomicron and very low-density lipoprotein remnants resulting from delayed lipolysis on the endothelium and impaired hepatic uptake. IDL in contrast to LDL is associated with vascular disease in dialysis patients. Lipoprotein (a) (Lp (a)) levels are also increased. In patients without renal disease. The concentration of Lp (a) is inversely associated with the size of the apolipoprotein (a) isoform inherited; Lp (a) levels are increased in patients with kidney disease as a consequence of increased concentrations, primarily of the high molecular weight isoform. Lp (a) levels are also associated with cardiovascular outcome among dialysis patients. |
Author | Kaysen, G.A. |
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Keywords | IDL CETP LCAT apo A I apo C III hepatic lipase |
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Title | Dyslipidemia in chronic kidney disease: Causes and consequences |
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