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非诺贝特可增加轻度肾功能不全患者的血肌酐,但不改变其肾小球滤过率。

[Fenofibrate increases blood creatinine, but does not change the glomerular filtration rate in patients with mild renal insufficiency].

作者信息

Hottelart C, el Esper N, Achard J M, Pruna A, Fournier A

机构信息

Service de néphrologie-médecine interne, CHU, Hôpital Sud, Amiens.

出版信息

Nephrologie. 1999;20(1):41-4.

Abstract

Fenofibrate is a potent hypolipemic agent, widely used in patients with mild to severe renal failure in whom hyperlipoproteinemia is frequent. A moderate reversible increase in creatinine plasma levels has been reported with fenofibrate therapy; however, it is not known whether this increased creatininemia reflects a fenofibrate induced alteration of renal function or if fenofibrate interferes with creatinine tubular handling. We prospectively examined the effect of 2 weeks fenofibrate treatment (200 mg daily) on renal function in thirteen hyperlipidemic patients with normal renal function or mild to moderate renal failure (Creat Cl: 110 to 30 ml/min). This study confirms that fenofibrate therapy significantly increases creatininemia in patients with mild to moderate renal failure (147 +/- 12 versus 170 +/- 15 mmol/l; p = 0.014), but does not alter renal hemodynamic nor glomerular filtration rate as assessed by the stability of PAH (304 +/- 56 versus 311 +/- 49 ml/min; p = NS) and inulin clearances (51.7 +/- 6 versus 52.3 +/- 7 ml/min; p = NS). The increase in creatininemia is neither due to an inhibition of creatinine tubular excretion, since no change in creatinine clearance was observed (69 +/- 8 versus 68 +/- 8 ml/min; p = NS), but appears to be associated to a parallel increase in creatinine daily urinary excretion (13.7 +/- 5 versus 15.4 +/- 4 mmol; p = 0.03). In conclusion, fenofibrate therapy in renal patients does not worsen renal function, nor diminish the reliability of creatinine clearance for its follow-up in spite of a significant rise in creatininemia. The mechanism of the fenofibrate-induced increase in urinary creatinine excretion remains to be determined.

摘要

非诺贝特是一种强效的降血脂药物,广泛应用于轻度至重度肾衰竭且经常发生高脂蛋白血症的患者。有报道称非诺贝特治疗会使血浆肌酐水平出现中度可逆性升高;然而,尚不清楚这种肌酐血症的增加是反映了非诺贝特诱导的肾功能改变,还是非诺贝特干扰了肌酐的肾小管处理过程。我们前瞻性地研究了13例肾功能正常或轻度至中度肾衰竭(肌酐清除率:110至30 ml/分钟)的高脂血症患者接受为期2周的非诺贝特治疗(每日200 mg)对肾功能的影响。本研究证实,非诺贝特治疗可使轻度至中度肾衰竭患者的肌酐血症显著增加(147±12对170±15 mmol/L;p = 0.014),但不会改变肾血流动力学或肾小球滤过率,这通过对氨基马尿酸(PAH)的稳定性评估(304±56对311±49 ml/分钟;p = 无显著性差异)和菊粉清除率(51.7±6对52.3±7 ml/分钟;p = 无显著性差异)得以体现。肌酐血症的增加并非由于肌酐肾小管排泄受到抑制,因为未观察到肌酐清除率有变化(69±8对68±8 ml/分钟;p = 无显著性差异),但似乎与肌酐每日尿排泄量的平行增加有关(13.7±5对15.4±4 mmol;p = 0.03)。总之,尽管肌酐血症显著升高,但非诺贝特治疗肾病患者并不会使肾功能恶化,也不会降低肌酐清除率在随访中的可靠性。非诺贝特诱导尿肌酐排泄增加的机制仍有待确定。

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