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大鼠急性高尿酸血症肾病。一项电子显微镜研究。

Acute hyperuricemic nephropathy in rats. An electron microscopic study.

作者信息

Waisman J, Mwasi L M, Bluestone R, Klinenberg J R

出版信息

Am J Pathol. 1975 Nov;81(2):367-78.

Abstract

Hyperuricemia and uricosuria were induced in rats fed uric acid and oxonic acid. Kidneys then were studied by light and electron microscopy. After 1 day of hyperuricemia, animals had deposits of uric acid and urate crystals within collecting tubules of the renal papillae, and tubular cells were altered. By 10 days, there was an exudative response with further injury to epithelium. Clear spaces within lumens, epithelium, and neutrophils suggested the presence of crystals; however, there was no direct ultrastructural evidence that neutrophils or epithelial cells ingested crystals and suffered injury. Presumably, crystals readily seen in frozen, unfixed tissue were lost during preparation for electron microscopy. Nonetheless, the ultrastructural findings indicated that hyperuricemic nephropathy was initiated in a fashion analogous to urate arthropathy. Urate crystals formed within collecting tubules, epithelial cells were altered, and most likely there was chemotaxis of neutrophils which underwent degranulation and vacuolation followed by lysis freeing any ingested urate. Release of ingested crystals plus precipitation of new crystals both might serve to sustain the nephritis.

摘要

给喂食尿酸和氧嗪酸的大鼠诱发高尿酸血症和尿酸尿症。然后用光镜和电镜研究肾脏。高尿酸血症1天后,动物肾乳头集合管内有尿酸和尿酸盐结晶沉积,肾小管细胞发生改变。到第10天,出现渗出反应,上皮进一步损伤。管腔、上皮内的清亮间隙和中性粒细胞提示有结晶存在;然而,没有直接的超微结构证据表明中性粒细胞或上皮细胞摄取了结晶并受到损伤。推测在冷冻的未固定组织中容易看到的结晶在电子显微镜标本制备过程中丢失了。尽管如此,超微结构结果表明高尿酸血症肾病的起始方式类似于尿酸盐关节病。尿酸盐结晶在集合管内形成,上皮细胞发生改变,很可能有中性粒细胞趋化作用,中性粒细胞发生脱颗粒和空泡化,随后溶解,释放出摄取的任何尿酸盐。摄取的结晶释放加上新结晶的沉淀都可能维持肾炎。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be22/2032218/f8462079ff1d/amjpathol00456-0124-a.jpg

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