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硫酸铜中毒后急性肾衰竭。

Acute renal failure following copper sulphate intoxication.

作者信息

Chugh K S, Sharma B K, Singhal P C, Das K C, Datta B N

出版信息

Postgrad Med J. 1977 Jan;53(615):18-23. doi: 10.1136/pgmj.53.615.18.

DOI:10.1136/pgmj.53.615.18
PMID:876909
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2496546/
Abstract

Eleven out of a series of twenty-nine patients (37-9%) with acute copper sulphate poisoning developed acute renal failure. Intravascular haemolysis appeared to be the chief factor responsible for renal lesions in these patients. Histological lesions observed in the kidney varied from those of mild shock to well established acute tubular necrosis. In one case, granulomatous lesions were seen in response to tubulorrhexis. Renal failure was the chief indication for dialysis in ten patients, whereas one patient was dialysed primarily for removal of copper. Notwithstanding the adequate control of uraemia by dialysis, only six of the eleven patients recovered. Septicaemia was responsible for death in three, hepatic failure in one and methaemoglobinaemia in another. It is postulated that release of copper from haemolysed red cells during acute haemolytic episodes may initiate, or contribute to, the development of renal damage.

摘要

在29例急性硫酸铜中毒患者中,有11例(37.9%)发生了急性肾衰竭。血管内溶血似乎是这些患者肾脏损伤的主要原因。在肾脏观察到的组织学病变从轻度休克到典型的急性肾小管坏死不等。有1例患者,因肾小管破裂出现肉芽肿性病变。肾衰竭是10例患者进行透析的主要指征,而有1例患者主要是为了清除铜而进行透析。尽管通过透析充分控制了尿毒症,但11例患者中只有6例康复。3例患者死于败血症,1例死于肝衰竭,另1例死于高铁血红蛋白血症。据推测,急性溶血发作期间溶血红细胞释放的铜可能引发或促成肾损伤的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d68/2496546/0b48c8588b7a/postmedj00265-0023-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d68/2496546/7e9f44be2c3a/postmedj00265-0022-a.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d68/2496546/e8386a136212/postmedj00265-0023-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d68/2496546/0b48c8588b7a/postmedj00265-0023-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d68/2496546/7e9f44be2c3a/postmedj00265-0022-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d68/2496546/fa4506ee07dc/postmedj00265-0023-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d68/2496546/e8386a136212/postmedj00265-0023-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d68/2496546/0b48c8588b7a/postmedj00265-0023-c.jpg

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