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严重草酸钙肾结石中正常草酸钙晶体生长抑制

Normal calcium oxalate crystal growth inhibition in severe calcium oxalate nephrolithiasis.

作者信息

Porile J L, Asplin J R, Parks J H, Nakagawa Y, Coe F L

机构信息

Nephrology Section, University of Chicago School of Medicine, IL. 60637, USA.

出版信息

J Am Soc Nephrol. 1996 Apr;7(4):602-7. doi: 10.1681/ASN.V74602.

Abstract

Urine from mammalian kidneys is regularly supersaturated with respect to calcium oxalate monohydrate, the most common solid phase in human nephrolithiasis, and also inhibits the nucleation, growth, and aggregation of calcium oxalate crystals. Nephrolithiasis is often associated with increased supersaturation, and it is assumed that this increase overbalances the inhibition effects, causing stones. However, some patients form stones in the absence of increased supersaturation, and in those patients, one might assume that reduced inhibition is the cause of their stones. This hypothesis was tested in 25 patients who formed at least ten stones each, yet lacked the usual metabolic abnormalities that increase supersaturation. Compared with 25 age- and sex-matched control subjects, urine supersaturation among the patients was not increased; this is an expected result of this study's selection criteria. Compared with the same age- and sex-matched control subjects, urine from the patients showed no evidence for reduced inhibition of calcium oxalate crystal growth, so low inhibition of growth did not contribute to pathogenesis of stones in our highly selected study population, despite their otherwise unexplained and active stone formation. These results do not support the hypothesis that growth inhibition defects are a cause of stone disease.

摘要

哺乳动物肾脏产生的尿液相对于一水合草酸钙经常处于过饱和状态,一水合草酸钙是人类肾结石中最常见的固相,并且还抑制草酸钙晶体的成核、生长和聚集。肾结石通常与过饱和度增加有关,据推测这种增加超过了抑制作用,从而导致结石形成。然而,一些患者在没有过饱和度增加的情况下也会形成结石,对于这些患者,有人可能会认为抑制作用减弱是他们患结石的原因。在25名每人至少形成10颗结石但缺乏通常会增加过饱和度的代谢异常的患者中对这一假设进行了检验。与25名年龄和性别匹配的对照受试者相比,患者的尿液过饱和度并未增加;这是本研究选择标准的预期结果。与相同年龄和性别匹配的对照受试者相比,患者的尿液没有显示出对草酸钙晶体生长抑制作用减弱的证据,因此在我们经过高度筛选的研究人群中,尽管他们存在无法解释的活跃结石形成情况,但生长抑制作用降低对结石发病机制并无贡献。这些结果不支持生长抑制缺陷是结石病病因的假设。

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