, not specific to CKD) demonstrated a modest 10% relative risk reduction in major cardiovascular events and a 13% relative risk reduction in coronary events for fibrate therapy.38 Too few participants with eGFR o60 ml/min per 1.73 m2 were included in either FIELD (The Fenofibrate Intervention and Event Lowering in Diabetes) or ACCORD-Lipid (Action to Control Cardiovascular Risk in Diabetes-Lipid) to provide reliable information on either the safety or efficacy of fenofibrate in this group. Allocation to fenofibrate in the FIELD study was associated with an increased risk of doubling of plasma creatinine, which cannot simply be explained by the small step-rise in creatinine due to fenofibrate. A recent large observational study in patients aged 466 years demonstrated a clear association between new C review prescriptions for fibric acid derivatives and increased serum creatinine levels, as well as a small increase in the risk of hospitalization and nephrologist consultation.39 These findings contribute to the uncertainty that fibric acid derivatives would yield net clinical benefit in people with CKD. For these reasons, the use of fibric acid derivatives to reduce cardiovascular risk is not recommended in patients with CKD. Fibric acid derivatives could be considered for the rare patients with CKD and markedly elevated fasting levels of serum TGs (411.3 mmol/l (41000 mg/dl)). If such therapy is prescribed, fibric acid derivatives must be dose-adjusted for kidney function. Concomitant therapy with both a fibric acid derivative and a statin is not recommended in patients with CKD owing to the potential for toxicity. Non-pharmacological treatment of high TGs (4500 mg/ dl; 5.65 mmol/l) includes therapeutic lifestyle changes such as dietary modification, weight reduction, increased physical activity, reducing alcohol intake, and treatment of hypergly- cemia (if present). 