Cardiovascular disease is increased in patients with chronic kidney disease (CKD) and is the principle cause of morbidity and mortality in these patients. Dyslipidemia, while common in these patients, is usually not characterized by elevated cholesterol, except in those patients with massive proteinuria. Qualitatively, increased triglycerides and reduced high-density lipoproteins (HDL) are most frequently described. Extensive abnormalities in the metabolism of apolipoprotein (apo) B-containing lipoproteins have been demonstrated, including those derived from the gut (apoB-48) as well as those derived from hepatic synthesis (apoB-100). Decreased enzymatic delipidation, in addition to reduced receptor removal of these lipoproteins, results in increased concentrations of these apoB-containing moieties, and in particular, their atherogenic remnants. Abnormalities in apoA-containing lipoproteins are also present and these changes may contribute not only to the lower levels of HDL seen, but also to the proinflammatory state that is frequently present in CKD patients. As a result, therapeutic strategies designed to modify atherosclerotic-caused outcomes in CKD may require multiple approaches.
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