BACKGROUND: Some reports indicate that fibrates can induce renal dysfunction. However, the clinical characteristics of these episodes, and the respective nephrotoxicity of the four main fibrates used-namely, fenofibrate, bezafibrate, ciprofibrate, and gemfibrozil-remain ill defined. METHODS: To better characterize this side-effect, we first reviewed the charts of 27 patients from our institution who developed an impairment of renal function during fibrate therapy. We next analysed the articles (n=24) that contained data on renal function in patients taking fibrates (n=2676). RESULTS: Among our 27 patients, 25 were on fenofibrate therapy, one was taking bezafibrate, and one ciprofibrate. Nineteen were recipients of solid-organ transplants (kidney recipients, n=15; heart or heart-lung recipients, n=4), and eight were non-transplanted patients with some impairment of renal function. Baseline plasma creatinine ranged from 0.9 to 2.9 mg/dl. It increased by a mean of 40% after the start of fibrate therapy. There was a concomitant increase of blood urea values (mean 36%) in most of the patients. Renal function returned to baseline in 18/24 patients after fibrate discontinuation. However, six patients, all transplant recipients, experienced a permanent increase in plasma creatinine. The incidence of fibrate-induced renal dysfunction among our series of kidney transplant recipients was 60%, as it occurred in 15 of the 25 patients who had ever taken fibrates. An increase of mean creatinine values during therapy was described in all papers on fenofibrate (n=7) and bezafibrate (n=8) (range 8-18% and 8-40% respectively), and in three of four papers dealing with ciprofibrate (range 6-16%). No significant renal impairment was described in any of the eight articles reporting data on gemfibrozil therapy. CONCLUSION: Therapy with fenofibrate, bezafibrate, and ciprofibrate may induce renal dysfunction. Gemfibrozil appears to be devoid of this side-effect.
BACKGROUND: Some reports indicate that fibrates can induce renal dysfunction. However, the clinical characteristics of these episodes, and the respective nephrotoxicity of the four main fibrates used-namely, fenofibrate, bezafibrate, ciprofibrate, and gemfibrozil-remain ill defined. METHODS: To better characterize this side-effect, we first reviewed the charts of 27 patients from our institution who developed an impairment of renal function during fibrate therapy. We next analysed the articles (n=24) that contained data on renal function in patients taking fibrates (n=2676). RESULTS: Among our 27 patients, 25 were on fenofibrate therapy, one was taking bezafibrate, and one ciprofibrate. Nineteen were recipients of solid-organ transplants (kidney recipients, n=15; heart or heart-lung recipients, n=4), and eight were non-transplanted patients with some impairment of renal function. Baseline plasma creatinine ranged from 0.9 to 2.9 mg/dl. It increased by a mean of 40% after the start of fibrate therapy. There was a concomitant increase of blood urea values (mean 36%) in most of the patients. Renal function returned to baseline in 18/24 patients after fibrate discontinuation. However, six patients, all transplant recipients, experienced a permanent increase in plasma creatinine. The incidence of fibrate-induced renal dysfunction among our series of kidney transplant recipients was 60%, as it occurred in 15 of the 25 patients who had ever taken fibrates. An increase of mean creatinine values during therapy was described in all papers on fenofibrate (n=7) and bezafibrate (n=8) (range 8-18% and 8-40% respectively), and in three of four papers dealing with ciprofibrate (range 6-16%). No significant renal impairment was described in any of the eight articles reporting data on gemfibrozil therapy. CONCLUSION: Therapy with fenofibrate, bezafibrate, and ciprofibrate may induce renal dysfunction. Gemfibrozil appears to be devoid of this side-effect.
Authors: K Sarat Chandra; Manish Bansal; Tiny Nair; S S Iyengar; Rajeev Gupta; Subhash C Manchanda; P P Mohanan; V Dayasagar Rao; C N Manjunath; J P S Sawhney; Nakul Sinha; A K Pancholia; Sundeep Mishra; Ravi R Kasliwal; Saumitra Kumar; Unni Krishnan; Sanjay Kalra; Anoop Misra; Usha Shrivastava; Seema Gulati Journal: Indian Heart J Date: 2014-12-24
Authors: Konstantinos Tziomalos; Emmanuel S Ganotakis; Irene F Gazi; Devaki R Nair; Dimitri P Mikhailidis Journal: Open Cardiovasc Med J Date: 2009-06-16