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布洛芬相关的肾功能障碍。急性肾衰竭、高钾血症、肾小管坏死和蛋白尿的病理生理机制。

Ibuprofen-associated renal dysfunction. Pathophysiologic mechanisms of acute renal failure, hyperkalemia, tubular necrosis, and proteinuria.

作者信息

Marasco W A, Gikas P W, Azziz-Baumgartner R, Hyzy R, Eldredge C J, Stross J

机构信息

Department of Pathology, University of Michigan Medical School, Ann Arbor 48109.

出版信息

Arch Intern Med. 1987 Dec;147(12):2107-16. doi: 10.1001/archinte.147.12.2107.

DOI:10.1001/archinte.147.12.2107
PMID:3689062
Abstract

Ibuprofen-associated, acute, reversible renal failure with hyperkalemia, tubular necrosis, and proteinuria developed in a patient who had no predisposing underlying disease. A renal biopsy specimen revealed mesangial hypercellularity without glomerular crescent formation. A profound interstitial nephritis with focal inflammatory cell infiltrates of predominantly mononuclear cells and neutrophils as well as focal tubular destruction was seen. Vasculitis was not observed. Ultrastructural studies confirmed the light microscopic diagnosis of a tubulointerstitial nephritis and, in addition, indicated the presence of electron-dense mesangial and subepithelial deposits. Direct immunofluorescence examination showed diffuse mesangial IgM and C3 deposition as well as vascular C3 deposition. Renal failure rapidly resolved after discontinuation of ibuprofen therapy and initiation of steroid therapy, with return to normal levels of serum creatinine, urea nitrogen, potassium, and sodium. Proteinuria also resolved.

摘要

一名无基础疾病易患因素的患者发生了与布洛芬相关的急性可逆性肾衰竭,伴有高钾血症、肾小管坏死和蛋白尿。肾活检标本显示系膜细胞增多,无肾小球新月体形成。可见严重的间质性肾炎,伴有以单核细胞和中性粒细胞为主的局灶性炎性细胞浸润以及局灶性肾小管破坏。未观察到血管炎。超微结构研究证实了光镜下肾小管间质性肾炎的诊断,此外,还显示存在电子致密的系膜和上皮下沉积物。直接免疫荧光检查显示弥漫性系膜IgM和C3沉积以及血管C3沉积。停用布洛芬治疗并开始使用类固醇治疗后,肾衰竭迅速缓解,血清肌酐、尿素氮、钾和钠水平恢复正常。蛋白尿也消失了。

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