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高钙尿症大鼠中过饱和度与晶体抑制之间的关系。

Relationship between supersaturation and crystal inhibition in hypercalciuric rats.

作者信息

Asplin J R, Bushinsky D A, Singharetnam W, Riordon D, Parks J H, Coe F L

机构信息

Nephrology Program, University of Chicago, Illinois, USA.

出版信息

Kidney Int. 1997 Mar;51(3):640-5. doi: 10.1038/ki.1997.93.

DOI:10.1038/ki.1997.93
PMID:9067894
Abstract

Calcium oxalate (CaOx) and calcium phosphate (CaP) crystals do not precipitate in large amounts in normal urine despite considerable supersaturation (SS), partly because urine inhibits crystal nucleation, aggregation, and growth. In normal rats and rats bred for hypercalciuria (GHS), we varied SS by varying calcium intake to test the hypothesis that increased SS might deplete inhibitors and reduce inhibition of crystal formation. In normal rats when compared to a low calcium diet (0.02% Ca), a high calcium diet (1.2% Ca) raised the SS of CaOx from 0.8 to 8.2. The high calcium diet also raised the upper limit of metastability (ULM) of CaOx (the SS at which crystals form in urine) from 11.8 to 36. In GHS rats, diet change altered CaOx SS from 1.5 to 12, and ULM from 17 to 50 (all differences, P < 0.001). Because ULM rose with SS, the increased SS had little potential to increase CaOx stone risk. For CaP, however, SS rose from 0.6 to 2.4 and 1.1 to 8 in normal and GHS rats (P < 0.001 for both), respectively, whereas ULM for CaP did not increase significantly (8 vs. 7 and 7 vs. 11; P = NS, both changes). Therefore, CaP SS rose close to the ULM, posing a high stone risk. The stones formed by these rats are composed of CaP. Increasing CaOx SS by diet raises ULM for CaOx thereby offsetting the risk of CaOx stones in rats.

摘要

尽管存在相当程度的过饱和(SS),草酸钙(CaOx)和磷酸钙(CaP)晶体在正常尿液中并不会大量沉淀,部分原因是尿液会抑制晶体的成核、聚集和生长。在正常大鼠和因高钙尿症而培育的大鼠(GHS)中,我们通过改变钙摄入量来改变SS,以检验增加的SS可能会耗尽抑制剂并降低对晶体形成的抑制作用这一假设。与低钙饮食(0.02%钙)相比,正常大鼠采用高钙饮食(1.2%钙)时,CaOx的SS从0.8提高到了8.2。高钙饮食还将CaOx的亚稳上限(ULM,即尿液中晶体形成时的SS)从11.8提高到了36。在GHS大鼠中,饮食变化使CaOx的SS从1.5变为12,ULM从17变为50(所有差异,P < 0.001)。由于ULM随SS升高,增加的SS几乎没有增加CaOx结石风险的可能性。然而,对于CaP,正常大鼠和GHS大鼠的SS分别从0.6升至2.4和从1.1升至8(两者P均< 0.001),而CaP的ULM没有显著增加(分别为8对7和7对11;P =无显著性差异,两种变化均如此)。因此,CaP的SS接近ULM升高,带来了较高的结石风险。这些大鼠形成的结石由CaP组成。通过饮食增加CaOx的SS会提高CaOx的ULM,从而抵消大鼠中CaOx结石的风险。

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