Physiology and Biophysics Department, Instituto de Investigaciones Metabólicas, Universidad del Salvador, Libertad 836, 1 piso, 1012, Buenos Aires, Argentina.
Int Urol Nephrol. 2018 May;50(5):879-883. doi: 10.1007/s11255-017-1784-7. Epub 2018 Jan 17.
In recent years, the role of trace elements in lithogenesis has received steadily increasing attention. It is well documented that some trace elements can influence the morphology and speed of the crystallization process. Zinc has been found in significant amounts in calcium stones relative or organic stones (uric acid and cystine), probably substituting calcium in crystals because of their similarity in charge and size. High Zn levels are present in carbapatite of Randal's plaques suggesting that zinc could promote calcium phosphate deposition in the medullar interstitium. Large-scale epidemiological studies have found an association of increased dietary zinc intake with increased risk of nephrolithiasis in adults but not in adolescents. Most studies examining urinary zinc levels in adults have reported increased urinary Zn excretion in stone formers. In an experimental model of organic crystal formation produced by silencing xanthine dehydrogenase in Drosophila fly, maneuvers that reduce Zn excretion have shown to reduce crystal formation in the lumen of the Malpighian tubules. This is curious because this is not a model of calcium stone formation. Finally, zinc supplementation has been associated with increased admissions for urinary lithiasis in men, but no change in calcium stone formation in children. Perhaps, some of these contradicting findings can be explained in part by the in vitro effect of zinc on the type and amount of calcium phosphate formed: At low concentrations, Zn inhibited the crystal growth of dicalcium phosphate dihydrate, octacalcium phosphate, and apatite, and at higher concentrations, it promoted the formation of amorphous calcium phosphate. Thus, further studies are needed to see whether manipulation of Zn metabolism can inhibit calcium stone formation.
近年来，微量元素在结石形成中的作用受到了越来越多的关注。有大量文献记载表明，某些微量元素可以影响结晶过程的形态和速度。锌在钙结石（相对或有机结石，如尿酸和胱氨酸）中含量丰富，可能由于其电荷和大小相似而替代了晶体中的钙。Randall 斑块的碳磷灰石中存在高锌水平，表明锌可能促进了肾髓质间质中磷酸钙的沉积。大规模的流行病学研究发现，成年人膳食中锌摄入量增加与肾结石风险增加有关，但青少年则没有。大多数研究报告称，结石形成者的尿锌排泄增加。在通过沉默黄嘌呤脱氢酶在果蝇中产生的有机晶体形成的实验模型中，减少锌排泄的操作已被证明可减少马氏管腔中的晶体形成。这很奇怪，因为这不是钙结石形成的模型。最后，锌补充剂与男性尿结石住院人数增加有关，但对儿童钙结石形成没有影响。也许，部分这些相互矛盾的发现可以部分解释为锌对形成的磷酸钙的类型和数量的体外作用：在低浓度下，Zn 抑制了二水合磷酸氢钙、八钙磷酸盐和磷灰石的晶体生长，而在较高浓度下，它促进了无定形磷酸钙的形成。因此，需要进一步研究以确定是否可以通过操纵 Zn 代谢来抑制钙结石形成。
