Neyer U, Wöss E, Bürgin M, Hofmann E, Möst J
Schweiz Med Wochenschr. 1985 Nov 2;115(44):1551-5.
A 59-year-old man developed a nephrotic syndrome and mild renal failure after treatment with phenylbutazone. Light microscope examination of a renal biopsy specimen showed minimal glomerular alterations, and electron microscopy showed diffuse fusion of epithelial cell foot processes without immune deposits. The interstitium revealed focal lymphocyte infiltrates identified as activated T-cells by immune histologic differentiation. The unusual combination of nephrotic syndrome with acute interstitial nephritis is a rare adverse reaction of nonsteroidal antiinflammatory drugs (NSAID). A disordered cell-mediated immunity could lead to interstitial infiltration of T-lymphocytes which, releasing lymphokines and a vascular permeability factor, cause the glomerular proteinuria. In addition, NSAID inhibition of prostaglandin synthesis may enhance production of these lymphocyte-derived substances. Since the nephrotic syndrome persisted 5 months after withdrawal of phenylbutazone, steroid therapy was initiated and 2 months later the renal insufficiency and proteinuria were resolved.
一名59岁男性在使用保泰松治疗后出现肾病综合征和轻度肾衰竭。对肾活检标本进行光镜检查显示肾小球改变轻微，电镜检查显示上皮细胞足突弥漫性融合，无免疫沉积物。间质可见局灶性淋巴细胞浸润，通过免疫组织学鉴别确定为活化的T细胞。肾病综合征与急性间质性肾炎的不寻常组合是非甾体抗炎药（NSAID）罕见的不良反应。细胞介导的免疫紊乱可导致T淋巴细胞间质浸润，T淋巴细胞释放淋巴因子和血管通透性因子，从而引起肾小球蛋白尿。此外，NSAID对前列腺素合成的抑制可能会增强这些淋巴细胞衍生物质的产生。由于在停用保泰松后肾病综合征持续了5个月，因此开始使用类固醇治疗，2个月后肾功能不全和蛋白尿得到缓解。
