The short term effects of bezafibrate on the hypertriglyceridaemia of moderate to severe uraemia.

Ar, Williams; Baker, F.; Walls, John

doi:10.1111/j.1365-2125.1984.tb02477.x

Cited by 28 publications

(13 citation statements)

References 20 publications

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“…20 The result of the present study was consistent with that of this study. In the FIELD study, creatinine levels were significantly lower in the fenofibrate group than in the placebo group at 8 weeks after withdrawal of study drugs and it was suggested that fenofibrate had renoprotective effect in conjunction with the effect on albuminuria.…”

Section: Discussionsupporting

confidence: 83%

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Effect of Long-term Fenofibrate Therapy on Serum Creatinine and Its Reversibility in Hypertriglyceridemic Patients with Hypertension

Park

Jung

Kim

et al. 2017

J Lipid Atheroscler

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Objective: Previous studies have shown that fenofibrate therapy increases serum creatinine level and that there is a return of serum creatinine to baseline level after the discontinuation of the drug. We evaluated the effect of long-term fenofibrate therapy on creatinine levels and its reversibility in patients with hypertension and hypertriglyceridemia. Methods: This retrospective study enrolled 54 hypertensive and hypertriglyceridemic patients taking fenofibrate for 3-6 years (Fenofibrate group) and 30 control patients with similar age, sex, follow-up duration, and creatinine levels (Control group). In 23 patients taking fenofibrate with low triglyceride level and/or with high creatinine levels, fenofibrate was discontinued, and creatinine levels were measured after 2 months. Results: Creatinine levels increased in both the fenofibrate group (from 0.91±0.18 mg/dL to 1.09±0.23 mg/dL, p<0.001) and the control group (from 0.94±0.16 mg/dL to 0.98±0.16 mg/dL, p=0.04) compared to baseline. However, the elevation was more pronounced in the fenofibrate group than in the control group (21.1±15.4% vs. 4.5±11.3%, p<0.001). The discontinuation of fenofibrate lowered creatinine levels (from 1.39±0.32 mg/dL to 1.15±0.24 mg/dL, p<0.001) which were still higher than pre-treatment levels (p=0.013). Conclusion: Long-term fenofibrate therapy significantly increased creatinine levels in hypertensive and hypertriglyceridemic patients. The effect of fenofibrate on creatinine level was partially reversible. This finding suggests that follow-up creatinine level is necessary with fenofibrate therapy. (J Lipid Atheroscler 2017 December;6(2):89-96)

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Section: Discussionsupporting

confidence: 83%

“…19 Previous studies have reported that creatinine levels decreased after stopping fenofibrate. 19,20 However, it is unclear whether the reversibility is complete or partial.…”

Section: Discussionmentioning

confidence: 99%

Effect of Long-term Fenofibrate Therapy on Serum Creatinine and Its Reversibility in Hypertriglyceridemic Patients with Hypertension

Park

Jung

Kim

et al. 2017

J Lipid Atheroscler

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“…Although the use of bezafibrate in uraemic patients not yet receiving dialy sis [6,7] or maintained on haemodialysis [5] has been reported, our study is unique in three aspects: (1) we have included only CAPD patients; (2) we have used bezafi brate in its sustained-release form. Given at 400 mg/day, the drug caused severe toxicity.…”

Section: Discussionmentioning

confidence: 99%

“…Ischaemic heart disease still claims many lives on dialysis [2]. High-density lipoprotein cholesterol (HDL-C), thought to be protective against atherogenesis [3], is markedly reduced in uraemic patients and in those on continuous ambulatory peritoneal dialysis [4] (CAPD) [1], The Helsinki Heart Study [4] has shown that a reduction of ischaemic heart events during treatment with gemfi brozil is associated with an increase in serum HDL-C. Bezafibrate, a clofibric acid derivative, has been shown to increase HDL-C in uraemic patients [5][6][7]. A sustainedrelease form of the drug is now available, and the follow ing article describes an open study of the effect of sus tained-release bezafibrate on lipid metabolism in CAPD patients.…”

Section: Introductionmentioning

confidence: 99%

Sustained-Release Bezafibrate Corrects Lipid Abnormalities in Patients on Continuous Ambulatory Peritoneal Dialysis

1990

Nephron

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A study was undertaken in 24 Chinese patients on maintenance continuous ambulatory peritoneal dialysis, using bezafibrate in its sustained-release form to correct lipid abnormalities. Six patients who received 400 mg/day developed severe muscle weakness with grossly elevated creatine phosphokinase activities within 3 weeks. The drug was discontinued and the symptoms disappeared. The remaining 18 patients received 400 mg/week for 8 weeks. There was a significant decrease in serum triglyceride (2.74 ± 0.33 to 1.86 ± 0.17 mmol/l at the 4th week and 1.65 ± 0.4 mmol/l at the 8th week). Concomitantly, serum total cholesterol decreased. Serum high-density lipoprotein cholesterol increased significantly (from 1.18 ± 0.082 to 1.36 ± 0.060 mmol/l at the 4th week and 1.40 ± 0.103 mmol/l at the 8th week). Post-heparin lipoprotein and hepatic Upases were measured by a substrate-specific method. The former increased significantly (p = 0.000) after bezafibrate treatment while the latter did not change. All parameters of lipid metabolism returned towards baseline 4 weeks after discontinuation of therapy. The drug was well tolerated at 400 mg/week and there was no significant rise in serum creatine phosphokinase.

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“…This syndrome occurred in subjects with normal as well as impaired kidney function [5,6], Pharmacokinetic investi gations of bezafibrate in patients with chronic uremia showed that the half-life is significantly prolonged and renal clearance is markedly decreased [7], On the basis of these data, a dose adjustment has been suggested in patients with renal impairment. However, a significant increase in serum C K values, followed by reversion after drug withdrawal, has been reported despite the use of reduced dosages [8].…”

Section: Introductionmentioning

confidence: 99%

Bezafibrate-Induced Myopathy: No Evidence for Defects in Muscle Metabolism

Vita

Toscano

Mileto³

et al. 1993

Eur Neurol

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A 58-year-old man with chronic renal failure developed severe muscle pain and tenderness 1 week after starting bezafibrate 400 mg daily. Serum creatine kinase was 32,280 U/l. Muscle biopsy revealed scattered necrotic fibers and mild type 2b atrophy. Muscle total and free carnitine were at the upper limits of the normal range. Biochemical investigations of muscle homogenate showed normal carnitine pelmityl transferase (CPT) as well as normal individual glycolytic and mitochondrial enzyme activities. Withdrawal of the drug was followed by rapid clinical improvement. Our study casts doubt on the hypothesis that bezafibrate is able to affect muscle metabolic pathways. It is likely that the drug acts on cholesterol constituents of the muscle membrane, producing discontinuities of the sarcolemma and initiating cell necrosis.

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The short term effects of bezafibrate on the hypertriglyceridaemia of moderate to severe uraemia.

Cited by 28 publications

References 20 publications

Effect of Long-term Fenofibrate Therapy on Serum Creatinine and Its Reversibility in Hypertriglyceridemic Patients with Hypertension

Effect of Long-term Fenofibrate Therapy on Serum Creatinine and Its Reversibility in Hypertriglyceridemic Patients with Hypertension

Sustained-Release Bezafibrate Corrects Lipid Abnormalities in Patients on Continuous Ambulatory Peritoneal Dialysis

Bezafibrate-Induced Myopathy: No Evidence for Defects in Muscle Metabolism

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