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Nephrotoxicity of Germanium Compounds: Report of a Case and Review of the Literature

 

作者: A. Takeuchi,   N. Yoshizawa,   S. Oshima,   T. Kubota,   Y. Oshikawa,   Y. Akashi,   T. Oda,   H. Niwa,   N. Imazeki,   A. Seno,   Y. Fuse,  

 

期刊: Nephron  (Karger Available online 1992)
卷期: Volume 60, issue 4  

页码: 436-442

 

ISSN:1660-8151

 

年代: 1992

 

DOI:10.1159/000186805

 

出版商: S. Karger AG

 

关键词: Germanium;Nephrotoxicity

 

数据来源: Karger

 

摘要:

A 55-year-old woman was admitted to our hospital, complaining of general malaise, muscular weakness, anorexia and weight loss. She had a history of ingesting of a certain germanium (Ge) compound over the preceding 19 months, with a total dose of 47 g as Ge element. She was found to have renal failure (blood urea nitrogen, 44 mg/dl; serum creatinine, 2.6 mg/dl) without abnormal findings in urinalysis, and muscular and nervous damage. Initially, polymyositis was diagnosed and prednisolone administered. However, no improvement was seen, and neuromuscular symptoms and signs steadily worsened, ending in death. Microscopic study of the kidney showed that lipofuscin granules increased in the cells of the thick ascending limb of Henle’s loop to the distal convoluted tubule accompanying mild tubular atrophy and that some of the tubules of these segments had vacuolar degeneration or desquamation. No apparent glomerular and vascular changes were observed. High Ge content was found in serum, urine and various tissues, e.g., spleen, liver, kidney, adrenal gland and myocardium, while in controls Ge could not be detected in sera, urine or tissues. We also review case reports about Ge toxicity, and discuss the pathogenesis of renal failure induced by Ge compound

 

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