Kastrup J, Petersen P, Bartram R, Hansen J M
Br J Urol. 1985 Jun;57(3):265-8. doi: 10.1111/j.1464-410x.1985.tb06340.x.
The influence of trimethoprim on renal function has been investigated in two groups of volunteers, both without a history of either acute or chronic urinary tract disease. All had normal serum creatinine. They were treated with trimethoprim 200 mg bd for 14 days. In group A (median age 78 years), serum creatinine increased significantly from median 89 to 134 mumol/l (P less than 0.01) during the first week and returned to normal 1 week after termination of treatment to median 90 mumol/l (P less than 0.02). After 1 week's treatment in group B (median age 29 years), serum creatinine had increased significantly from median 87 to 107 mumol/l (P less than 0.05), remained stable in the second week and returned to the pre-treatment level 1 week after cessation of treatment: 87 mumol/l (P less than 0.05). The glomerular filtration rate determined by 51Cr-EDTA clearance did not change. There was a significant decrease in the 24-h endogenous creatinine clearance after 14 days' treatment from 111 to 87 ml/min/1.73 m2 (P less than 0.05). Our results are consistent with an age-independent reversible trimethoprim-induced inhibition of the tubular secretion of creatinine.
在两组均无急慢性泌尿系统疾病病史的志愿者中研究了甲氧苄啶对肾功能的影响。所有人血清肌酐均正常。他们接受了14天的甲氧苄啶治疗，剂量为每日两次，每次200毫克。在A组（中位年龄78岁）中，血清肌酐在第一周从中位数89显著升至134微摩尔/升（P<0.01），在治疗结束1周后恢复正常，中位数为90微摩尔/升（P<0.02）。在B组（中位年龄29岁）治疗1周后，血清肌酐从中位数87显著升至107微摩尔/升（P<0.05），在第二周保持稳定，并在停止治疗1周后恢复到治疗前水平：87微摩尔/升（P<0.05）。通过51Cr-EDTA清除率测定的肾小球滤过率没有变化。治疗14天后，24小时内源性肌酐清除率从111显著降至87毫升/分钟/1.73平方米（P<0.05）。我们的结果与甲氧苄啶诱导的与年龄无关的可逆性肌酐肾小管分泌抑制一致。
