Acute kidney injury (AKI) results from renal hemodynamic alterations, leading to reduced renal perfusion, direct toxicity to the renal tubule cells (acute tubular necrosis), tubulointerstitial inflammation secondary to an allergic reaction (acute interstitial nephritis), nephrolithiasis, or glomerulonephritis.1 AKI is specifically defined as:2-4 at least a 0.3 mg/dL increase in serum creatinine within 48 hours, 1.5 times increase in serum creatinine from baseline, or urine volume less than 0.5 mL/kg/hr for 6 continuous hours.

Hypertriglyceridemia, especially with serum triglycerides greater than 1,000 mg/dL, is a frequently cited risk factor for acute pancreatitis.1,2 Epidemiological evidence suggests that for every increase of approximately 100 mg/dL, absolute risk for hospitalization due to pancreatitis increases by 4%.1 Clinical practice guidelines suggest evaluating and treating triglyceride serum concentrations elevated at 500 mg/dL or greater.3,4 In addition to therapeutic lifestyle changes (i.e., 5 to 10% body weight reduction, decreasing added sugars and increasing unsaturated fats while eliminating trans fats, increasing exercise, abstinence from alcohol), pharmacological therapy with fibrates, niacin, omega-3 fatty acids, statins, and ezetimibe have been listed as potential triglyceride lowering therapies.3 Fenofibrate, associated with a 30 to 50% reduction in triglycerides, has been recommended for consideration for triglyceride lowering when concentrations are greater than 500 mg/dL, in combination with low- or moderate- intensity.