Smith C R, Lietman P S
Antimicrob Agents Chemother. 1983 Jan;23(1):133-7. doi: 10.1128/AAC.23.1.133.
We analyzed data from three prospective, controlled, randomized, double-blind clinical trails to determine whether furosemide increases the nephrotoxicity and auditory toxicity of aminoglycosides. All patients who received at least 72 h of treatment and who had no other cause for nephrotoxicity or auditory toxicity were included in the analysis. Nephrotoxicity developed in 10 of 50 (20.0%) patients given furosemide and in 38 of 222 (17.1%) patients not given furosemide (P greater than 0.3). Auditory toxicity developed in 5 of 23 patients (21.7%) given furosemide and in 28 of 119 patients (23.5%) not given furosemide (P greater than 0.3). In each case, the groups receiving and not receiving furosemide did not differ in mean age, initial creatinine, duration of aminoglycoside therapy, mean change in auditory acuity or creatinine, mean number of days to the development of toxicity, the frequency with which gentamicin, tobramycin, amikacin, or cephalothin was administered, or the mean predose and 1-h postdose plasma aminoglycoside levels. We conclude that furosemide use should not be considered a major risk factor for the development of aminoglycoside-induced nephrotoxicity or auditory toxicity.
我们分析了三项前瞻性、对照、随机、双盲临床试验的数据,以确定速尿是否会增加氨基糖苷类药物的肾毒性和耳毒性。所有接受至少72小时治疗且无其他肾毒性或耳毒性原因的患者均纳入分析。接受速尿治疗的50例患者中有10例(20.0%)发生肾毒性,未接受速尿治疗的222例患者中有38例(17.1%)发生肾毒性(P>0.3)。接受速尿治疗的23例患者中有5例(21.7%)发生耳毒性,未接受速尿治疗的119例患者中有28例(23.5%)发生耳毒性(P>0.3)。在每种情况下,接受和未接受速尿治疗的组在平均年龄、初始肌酐水平、氨基糖苷类药物治疗持续时间、听力或肌酐的平均变化、毒性发生的平均天数、庆大霉素、妥布霉素、阿米卡星或头孢噻吩的给药频率,或给药前及给药后1小时血浆氨基糖苷类药物水平方面均无差异。我们得出结论,使用速尿不应被视为氨基糖苷类药物引起肾毒性或耳毒性的主要危险因素。