Lipoprotein abnormalities such as low levels of high-density lipoprotein (HDL) and high triglycerides (TGs), associated with the metabolic syndrome, are also associated with subsequent decline in kidney function. Patients with end-stage kidney disease also exhibit low HDL and high TGs and a modest reduction in low-density lipoprotein (LDL), although the mechanisms responsible for these changes differ when patients with end-stage kidney disease are compared with those having metabolic syndrome with normal kidney function, as do lipoprotein structures. Among dialysis patients, oxidized LDL, levels of TG-rich intermediate-density lipoprotein, and low HDL are associated with aortic pulsewave velocity and other markers of atherosclerosis. Statins are effective in reducing LDL and do decrease risk of cardiovascular events in patients with CKD not requiring dialysis but have no significant effect on outcomes, including all-cause mortality among dialysis patients. Similarly gemfibrozil and other fibrates lower TGs, increase HDL, and reduce cardiovascular events, but not mortality, among patients with CKD not requiring dialysis but have no significant effect on cardiovascular outcomes in dialysis patients. There is potential clinical benefit in treating elevated LDL, TGs, and low HDL in patients with CKD using statins or fibrates in those not yet requiring dialysis.
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