Chronic renal insufficiency (CRI) is associated with a characteristic dyslipidemia. Findings in children with CRI largely parallel those in adults. Moderate hypertriglyceridemia, increased triglyceride-rich lipoproteins (TRL) and reduced high-density lipoproteins (HDL) are the most usual findings, whereas total and low-density lipoprotein cholesterol (LDL-C) remain normal or modestly increased. Qualitative abnormalities in lipoproteins are common, including small dense LDL, oxidized LDL, and cholesterol-enriched TRL. Measures of lipoprotein lipase and hepatic lipase activity are reduced, and concentrations of apolipoprotein C-III are
markedly elevated. Still an active area of research, major pathophysiological mechanisms leading to the dyslipidemia of CRI include insulin resistance and nonnephrotic proteinuria. Sources of variability in the severity of this dyslipidemia include the degree of renal impairment and the modality of dialysis. The benefits of maintaining normal body weight and physical activity extend to those with CRI. In addition to multiple hypolipidemic pharmaceuticals, fish oils are also effective as a triglyceride-lowering agent, and the phosphorous binding agent sevelamer also lowers LDL-C. Emerging classes of hypolipidemic agents and drugs affecting sensitivity to insulin may impact future treatment.

JM Saland, H. G. (2007). "Lipoprotein metabolism in chronic renal insufficiency." Pediatr Nephrol 22: 1095-1112.

Dyslipidemia is an important risk factor for cardiovascular disease and a likely mediator of CKD progression. Dyslipidemia in CRI manifests principally as increased
TG and decreased HDL, with nearly normal total cholesterol. Chylomicron and VLDL remnants have prolonged circulation and are found in increased levels among patients with CRI. HDL and its principal apolipoprotein, apoA-I, are reduced, probably as a consequence of elevated TRL. Insulin resistance, increased apoC-III, and impaired lipolysis are significant pathophysiological factors in this process, and nonnephrotic proteinuria is an indelible presence in this scenario. Statins, fish oil, fibrates, and agents reducing the intestinal absorption of cholesterol are examples of existing treatments that have normalizing effects on the lipid profile in CRI. Though data from some large, non-CKD-oriented trials of statins suggested reduced risk of ASCVD, others did not. Therefore, one must be cautious in drawing conclusions from these studies. With results from ongoing trials among individuals with CRI anticipated soon, more definitive recommendations should emerge, at least for adult patients. Development of pharmaceutical agents with novel activity on pathways central to the development of dyslipidemia in CRI offer exciting directions for future investigation.