Few clinical studies have also confirmed the renoprotective potential of fenofibrate against diabetic nephropathy. The 'Fenofibrate Intervention for Event Lowering in Diabetes (FIELD)' study suggested that fenofibrate treatment had promising effects in preventing the progression of diabetes-associated microvascular complications, including diabetic nephropathy [17-18]. In the FIELD study, among all type 2 diabetic patients (9795 patients), over 5 years, the fell of ACR was greater in participants on fenofibrate (23.7% vs 11.5%), albuminuria on average progressed 14% less frequently and was reversed 18% more often among those diabetic patients received fenofibrate as compared to placebo.The investigators of this trial suggested that fenofibrate could protect against the loss of underlying renal function seen in patients with T2DM[19].And also in ACCORD study[20], a lower incidence of both micro- and macro-albuminuria was noted in the fenofibrate compared with the placebo group [38.2 vs. 41.6% (P = 0.01) and 10.5 vs. 12.3% (P = 0.04), respectively]. Unfortunately, during fenofibrate therapy in FIELD study, the plasma creatinine was noted to be increased, but quickly reversed on placebo assignment. Though it remained higher on fenofibrate treatment as compared to placebo, the chronic rise was slower with less loss of estimated glomerular filtration rate (eGFR). How these short-term increases can affect long-term renal function was also assessed in a retrospective subanalysis of the ACCORD study[21]. Among fenofibrate-treated patients, 321 experienced increased SCr levels＞20% (cases) within the first 3 months of treatment. Patients with SCr increases ＜2% were controls (n = 175). In these patients as well as in 565 placebo-treated subjects, SCr and cystatin C levels were measured at baseline and 6-8 weeks after treatment discontinuation. As expected, cases had significantly higher SCr levels and lower eGFR than controls or placebo treated individuals at the end of the study. However, SCr levels and eGFR in cases returned to placebo levels 51 days after treatment discontinuation. At the same time, fenofibrate-treated patients with no initial increases in SCr levels had the lowest SCr levels and the highest eGFR. In the setting of careful renal function surveillance and reduction of fenofibrate dose as indicated, no increase in renal disease or cardiovascular outcome was seen in those individuals demonstrating fenofibrate-associated creatinine increase[22].Taken together, fenofibrate could delay albuminuria and eGFR impairment in T2DM patients. Of note, in a study reported by Hottelart et al. [23], fenofibrate associated increase in creatininemia in renal patients did not reflect an impairment of renal function. Fenofibrate-induced increase in creatinine production was suggested to be associated with an enhanced metabolic production rate of creatinine.