Fong H J, Cohen A H
Am J Nephrol. 1982;2(1):28-31. doi: 10.1159/000166578.
2 patients with systemic lupus erythematosus and mild renal functional impairment were treated with ibuprofen, one of the phenylproprionic nonsteroidal anti-inflammatory drugs. Within days after the onset of therapy, both developed renal insufficiency manifested by elevated serum creatinine levels, increased proteinuria, and active urinary sediments; 1 patient was oliguric. Renal biopsies disclosed mesangial proliferative lupus glomerulonephritis and acute tubular necrosis, the latter more pronounced in the oliguric patient. Renal failure resolved following discontinuation of ibuprofen and supportive therapy. It is postulated that altered blood flow, mediated through the well-known prostaglandin synthetase inhibitory effects of ibuprofen, resulted in tubular necrosis. This undesirable complication of ibuprofen therapy may be enhanced in patients with underlying renal disease, and may be a factor governing the limitation of its usage.
两名患有系统性红斑狼疮且伴有轻度肾功能损害的患者接受了布洛芬（一种苯丙酸类非甾体抗炎药）治疗。在治疗开始后的几天内，两人均出现肾功能不全，表现为血清肌酐水平升高、蛋白尿增加以及尿液中有活性沉积物；其中一名患者出现少尿。肾活检显示为系膜增生性狼疮性肾小球肾炎和急性肾小管坏死，后者在少尿患者中更为明显。停用布洛芬并给予支持治疗后，肾衰竭得以缓解。据推测，布洛芬通过其众所周知的抑制前列腺素合成酶的作用介导血流改变，从而导致肾小管坏死。布洛芬治疗的这种不良并发症在患有潜在肾脏疾病的患者中可能会加重，并且可能是限制其使用的一个因素。
