Department of Clinical Biochemistry, Frimley Park Hospital NHS Foundation Trust, Frimley, Surrey GUI6 JUJ, UK.
Ann Clin Biochem. 2012 Sep;49(Pt 5):491-3. doi: 10.1258/acb.2012.011163. Epub 2012 Jul 24.
The increase in creatinine in patients on fibrate therapy is well-recognized, but its mechanism is not clearly understood. A study by Hottelart et al. suggested that fibrate-induced creatininaemia was due to the effect of fibrates on creatinine metabolism as opposed to a decline in renal function. To address this hypothesis, we have monitored renal function in a group of hyperlipidaemic patients before commencing fibrate treatment and after three months of therapy.
We studied 12 subjects (10 men, 2 women), median age 43.5 y (range 33-70 y). Serum creatinine, cystatin C, creatine kinase and fasting lipids were measured.
We observed statistically significant increases in concentrations of serum creatinine (P < 0.005) and cystatin C(P < 0.01). Concentrations of both analytes increased in 10 (83.3%) of the patients. In these patients, the median increases were 15.1% (range 5.5-23.2%) for creatinine and 9.9% (range 1.1-26.1%) for cystatin C.
These results suggest that the decrease in estimated glomerular filtration rate, observed in patients undergoing fibrate therapy, is a genuine effect on kidney function rather than a change in creatinine metabolism as previously postulated, since the rises in serum creatinine concentration were reflected by rises in cystatin C, an independent marker of renal function.
在接受贝特类药物治疗的患者中,肌酸酐升高是众所周知的,但其机制尚不清楚。Hottelart 等人的一项研究表明,贝特类药物引起的肌酸酐血症是由于贝特类药物对肌酸酐代谢的影响,而不是肾功能下降。为了验证这一假设,我们在开始贝特类药物治疗前和治疗三个月后监测了一组高脂血症患者的肾功能。
我们研究了 12 名受试者(10 名男性,2 名女性),中位年龄 43.5 岁(范围 33-70 岁)。测量血清肌酐、胱抑素 C、肌酸激酶和空腹血脂。
我们观察到血清肌酐(P < 0.005)和胱抑素 C(P < 0.01)浓度有统计学显著升高。10 名患者(83.3%)的两种分析物浓度均升高。在这些患者中,肌酐中位数增加 15.1%(范围 5.5-23.2%),胱抑素 C 中位数增加 9.9%(范围 1.1-26.1%)。
这些结果表明,接受贝特类药物治疗的患者肾小球滤过率下降是对肾功能的真实影响,而不是先前假设的肌酸酐代谢变化,因为血清肌酐浓度的升高反映了胱抑素 C 的升高,胱抑素 C 是肾功能的独立标志物。