Dyslipidaemia in patients with chronic kidney disease and treatment

Introduction Treatment of dyslipidaemia complicated by chronic kidney disease is important for preventing the development of cardiovascular disease. The pathogenesis of dyslipidaemia associated with chronic kidney disease varies depending on urinary protein level and the stage of chronic kidney disease. Hypocholesterolaemia is associated with malnutrition and inflammation and also leads to the poor prognosis of dialysis patients. Statins are expected to prevent the development of cardiovascular disease in non-dialysis chronic kidney disease patients; however, there is no evidence of the efficacy of statins in preventing the development of cardiovascular disease in dialysis patients. Treatment strategies for dyslipidaemia in chronic kidney disease patients mainly include lifestyle changes, dietary therapies and medications such as statins; care should be taken with regard to the side effects of medicines. The aim of this article is to discuss dyslipidaemia in patients with chronic kidney disease. Conclusion Patients who showed abnormal findings in the lipid test should be treated by considering not only their test results but also their general condition including nutritional condition, medical history and complications. Personalised treatment of each patient, rather than across-the-board treatment, is necessary. Introduction Cardiovascular disease (CVD) is the leading cause of death in patients with chronic kidney disease (CKD) and must be prevented to improve their prognosis. Atherosclerosis is often a complication of CKD and adversely affects the prognosis of patients with CKD1–3. Dyslipidaemia is a cause of atherosclerosis. The relationship between pulse wave velocity (PWV) and very low-density lipoprotein cholesterol (VLDL-C), intermediate-density lipoprotein cholesterol (IDL-C), and low-density lipoprotein cholesterol (LDL-C) levels has been reported4. The Lipid lowering and Onset of Renal Disease (LORD) trial showed that atorvastatin suppressed the decrease in PWV5. The Atherosclerosis Risk in Communities (ARIC) study showed that hypercholesterolaemia and hypertriglyceridaemia are the risk factors for CVD6. Dyslipidaemia can develop at any stage of CKD and is a risk factor for CVD; hence, methods to control dyslipidaemia should be examined. This article discusses dyslipidaemia in patients with CKD and also the methods to treat these patients. Discussion Pathogenesis of dyslipidaemia The pathogenesis of dyslipidaemia associated with CKD varies depending on the urinary protein level and the stage of CKD7. For patients with nephrotic syndrome who have high urinary protein levels, albumin production is enhanced in the liver to compensate for hypoproteinaemia. At the same time, the synthesis of apolipoprotein (apo) B (apoB) is enhanced, resulting in elevated levels of VLDL-C and LDL-C. For patients with CKD who do not have as high urinary protein levels as those with nephrotic syndrome, dyslipidaemia is mainly caused by dysfunction in the catabolism of lipoproteins in the peripheral tissues. Patients with CKD at stage 3 or later show abnormal levels of lipoproteins and apolipoproteins, that is, decreased levels of apoA-I, apoA-II, and apoA-IV. The level of apoC-III, an inhibitor of lipoprotein lipase (LPL), is elevated and the apoA-I/apoC-III ratio decreases. With increasing apoCIII level, the production of VLDL, which is less affected by LPL activity, is enhanced, resulting in an elevated VLDL-C level. In CKD patients with diabetes mellitus, the production of triglycerides (TGs) is also enhanced because of diabetes mellitus, which overlaps with the above-mentioned pathologies. In dialysis patients (CKD stage 5D), LPL activity decreases because of the accumulation of uremic toxins and secondary hyperparathyroidism. Because hepatic triglyceride lipase activity also decreases, the conversion of IDLs to LDLs becomes difficult, resulting in elevated IDL levels and decreased LDL levels. The increase in IDL level leads to an increase in TG level. Although LDL level decreases, its plasma residence time increases, leading to degeneration caused by oxidation and accelerating atherosclerosis. Haemodialysis patients may have hypertriglyceridaemia and hypo-high-density * Corresponding author Email: [email protected] 1 Department of Nephrology, Tokyo Kyosai Hospital, Meguroku, Tokyo, Japan 2 Bioethics Research Center, Tokyo Medical and Dental University, Bunkyoku, Tokyo, Japan 3 Department of Nephrology, Tokyo Medical and Dental University, Bunkyoku, Tokyo, Japan